ki 67  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc ki 67
    EC-derived SO 2 deficiency activates HPAEC inflammation, HPASMC proliferation, and collagen synthesis in vitro . (a) Western blot analysis was performed to detect the expression level of AAT1 protein in HPAECs ( n = 12). (b) The red SO 2 fluorescent probe method was used to detect the SO 2 level in HPAECs; the nuclei were stained with DAPI. (c) Western blot analysis was used to detect the expression level of ICAM-1 and MCP-1 protein in HPAECs ( n = 12). (d) Immunofluorescence method was used to detect the expression level of ICAM-1 protein in HPAECs in situ . Purple fluorescence represents ICAM-1 protein. (e) Fluorescence method was conducted to detect the adhesion of THP-1 cells and HPAECs. The red Dil color marks the THP-1 cells, and the DAPI color marks the nuclei of HPAECs. (f) Diagram of the transwell used for the coculture system in vitro . (g) Western blot analysis method to detect the expression level of <t>Ki-67</t> and collagen I protein in HPASMCs cocultured with HPAECs ( n = 10). The data were expressed as mean ± SEM, ∗ p
    Ki 67, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 40 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Endothelial Cell-Derived SO2 Controls Endothelial Cell Inflammation, Smooth Muscle Cell Proliferation, and Collagen Synthesis to Inhibit Hypoxic Pulmonary Vascular Remodelling"

    Article Title: Endothelial Cell-Derived SO2 Controls Endothelial Cell Inflammation, Smooth Muscle Cell Proliferation, and Collagen Synthesis to Inhibit Hypoxic Pulmonary Vascular Remodelling

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2021/5577634

    EC-derived SO 2 deficiency activates HPAEC inflammation, HPASMC proliferation, and collagen synthesis in vitro . (a) Western blot analysis was performed to detect the expression level of AAT1 protein in HPAECs ( n = 12). (b) The red SO 2 fluorescent probe method was used to detect the SO 2 level in HPAECs; the nuclei were stained with DAPI. (c) Western blot analysis was used to detect the expression level of ICAM-1 and MCP-1 protein in HPAECs ( n = 12). (d) Immunofluorescence method was used to detect the expression level of ICAM-1 protein in HPAECs in situ . Purple fluorescence represents ICAM-1 protein. (e) Fluorescence method was conducted to detect the adhesion of THP-1 cells and HPAECs. The red Dil color marks the THP-1 cells, and the DAPI color marks the nuclei of HPAECs. (f) Diagram of the transwell used for the coculture system in vitro . (g) Western blot analysis method to detect the expression level of Ki-67 and collagen I protein in HPASMCs cocultured with HPAECs ( n = 10). The data were expressed as mean ± SEM, ∗ p
    Figure Legend Snippet: EC-derived SO 2 deficiency activates HPAEC inflammation, HPASMC proliferation, and collagen synthesis in vitro . (a) Western blot analysis was performed to detect the expression level of AAT1 protein in HPAECs ( n = 12). (b) The red SO 2 fluorescent probe method was used to detect the SO 2 level in HPAECs; the nuclei were stained with DAPI. (c) Western blot analysis was used to detect the expression level of ICAM-1 and MCP-1 protein in HPAECs ( n = 12). (d) Immunofluorescence method was used to detect the expression level of ICAM-1 protein in HPAECs in situ . Purple fluorescence represents ICAM-1 protein. (e) Fluorescence method was conducted to detect the adhesion of THP-1 cells and HPAECs. The red Dil color marks the THP-1 cells, and the DAPI color marks the nuclei of HPAECs. (f) Diagram of the transwell used for the coculture system in vitro . (g) Western blot analysis method to detect the expression level of Ki-67 and collagen I protein in HPASMCs cocultured with HPAECs ( n = 10). The data were expressed as mean ± SEM, ∗ p

    Techniques Used: Derivative Assay, In Vitro, Western Blot, Expressing, Staining, Immunofluorescence, In Situ, Fluorescence

    EC-derived SO 2 inhibits p50 activation to repress PAEC inflammation, PASMC proliferation, and collagen deposition. (a) Immunofluorescence in situ detection of p50 protein distribution in HPAECs. Red fluorescence represents p50 protein, and DAPI staining labels HPAEC nuclei. (b) Immunofluorescence in situ detection of p50 protein distribution in HPASMCs cocultured with HPAECs. Green fluorescence represents p50 protein, and DAPI staining labels HPASMC nuclei. (c) Western blot analysis was used to detect the expression level of ICAM-1 and MCP-1 protein in HPAECs ( n = 12). (d, e) Immunofluorescence in situ detection of Ki-67 and collagen I protein expression in HPASMCs cocultured with HPAECs. Green fluorescence represents Ki-67 and collagen I protein. Andro: andrographolide, an inhibitor of p50. Data were expressed as mean ± SEM, ∗ p
    Figure Legend Snippet: EC-derived SO 2 inhibits p50 activation to repress PAEC inflammation, PASMC proliferation, and collagen deposition. (a) Immunofluorescence in situ detection of p50 protein distribution in HPAECs. Red fluorescence represents p50 protein, and DAPI staining labels HPAEC nuclei. (b) Immunofluorescence in situ detection of p50 protein distribution in HPASMCs cocultured with HPAECs. Green fluorescence represents p50 protein, and DAPI staining labels HPASMC nuclei. (c) Western blot analysis was used to detect the expression level of ICAM-1 and MCP-1 protein in HPAECs ( n = 12). (d, e) Immunofluorescence in situ detection of Ki-67 and collagen I protein expression in HPASMCs cocultured with HPAECs. Green fluorescence represents Ki-67 and collagen I protein. Andro: andrographolide, an inhibitor of p50. Data were expressed as mean ± SEM, ∗ p

    Techniques Used: Derivative Assay, Activation Assay, Immunofluorescence, In Situ, Fluorescence, Staining, Western Blot, Expressing

    Increased EC-derived SO 2 ameliorates hypoxia-induced PAEC inflammation, PASMC proliferation, hypertrophy, and collagen production in vivo . (a) Immunofluorescence in situ detection of ICAM-1 protein expression in mouse PAECs; green fluorescence represents ICAM-1 protein. (b) Western blot analysis was performed to detect the expression level of ICAM-1 protein in mouse lung tissue ( n = 10). (c, d) Immunofluorescence in situ detection of Ki-67, α -SMA, and collagen I protein expression in mouse PASMCs; green fluorescence represents Ki-67 and collagen I protein, and red fluorescence represents α -SMA. The data were expressed as mean ± SEM, ∗ p
    Figure Legend Snippet: Increased EC-derived SO 2 ameliorates hypoxia-induced PAEC inflammation, PASMC proliferation, hypertrophy, and collagen production in vivo . (a) Immunofluorescence in situ detection of ICAM-1 protein expression in mouse PAECs; green fluorescence represents ICAM-1 protein. (b) Western blot analysis was performed to detect the expression level of ICAM-1 protein in mouse lung tissue ( n = 10). (c, d) Immunofluorescence in situ detection of Ki-67, α -SMA, and collagen I protein expression in mouse PASMCs; green fluorescence represents Ki-67 and collagen I protein, and red fluorescence represents α -SMA. The data were expressed as mean ± SEM, ∗ p

    Techniques Used: Derivative Assay, In Vivo, Immunofluorescence, In Situ, Expressing, Fluorescence, Western Blot

    2) Product Images from "Up-regulation of inflammation-related LncRNA-IL7R predicts poor clinical outcome in patients with cervical cancer"

    Article Title: Up-regulation of inflammation-related LncRNA-IL7R predicts poor clinical outcome in patients with cervical cancer

    Journal: Bioscience Reports

    doi: 10.1042/BSR20180483

    Knockdown of Lnc-IL7R inhibits the tumor growth of cervical cancer ( A ) The efficiency of knockdown in two cervical cancer cell lines Hela and SiHa was determined. ( B , C ) The cell vitalities and apoptosis of two cell lines were estimated by CCK-8 and Hoechst. ( D ) The expressions of BCL-2 and caspase-3 were assessed by western blot. ( E ) The mean tumor size (mm 3 ) was analyzed. ( F , G ) The expressions of Lnc-IL7R and Ki-67 proliferation index were estimated by Q-PCR and immunohistochemistry. *P
    Figure Legend Snippet: Knockdown of Lnc-IL7R inhibits the tumor growth of cervical cancer ( A ) The efficiency of knockdown in two cervical cancer cell lines Hela and SiHa was determined. ( B , C ) The cell vitalities and apoptosis of two cell lines were estimated by CCK-8 and Hoechst. ( D ) The expressions of BCL-2 and caspase-3 were assessed by western blot. ( E ) The mean tumor size (mm 3 ) was analyzed. ( F , G ) The expressions of Lnc-IL7R and Ki-67 proliferation index were estimated by Q-PCR and immunohistochemistry. *P

    Techniques Used: CCK-8 Assay, Western Blot, Polymerase Chain Reaction, Immunohistochemistry

    3) Product Images from "POU4F1 promotes the resistance of melanoma to BRAF inhibitors through MEK/ERK pathway activation and MITF up-regulation"

    Article Title: POU4F1 promotes the resistance of melanoma to BRAF inhibitors through MEK/ERK pathway activation and MITF up-regulation

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-020-2662-2

    The expression level of POU4F1 was associated with Ki-67 level and the progression of melanoma. a Representative immunohistochemistry staining images of Ki-67 and POU4F1 expressions in nevus and melanoma tissues, bar = 200 μm. b Quantitative analysis of Ki-67 staining score. c Quantitative analysis of POU4F1 staining score. (nevus n = 6, primary melanoma n = 10, metastatic melanoma n = 10) Data are mean ± SEM, ** p
    Figure Legend Snippet: The expression level of POU4F1 was associated with Ki-67 level and the progression of melanoma. a Representative immunohistochemistry staining images of Ki-67 and POU4F1 expressions in nevus and melanoma tissues, bar = 200 μm. b Quantitative analysis of Ki-67 staining score. c Quantitative analysis of POU4F1 staining score. (nevus n = 6, primary melanoma n = 10, metastatic melanoma n = 10) Data are mean ± SEM, ** p

    Techniques Used: Expressing, Immunohistochemistry, Staining

    4) Product Images from "The Anticancer Activity Conferred by the Mud Crab Antimicrobial Peptide Scyreprocin through Apoptosis and Membrane Disruption"

    Article Title: The Anticancer Activity Conferred by the Mud Crab Antimicrobial Peptide Scyreprocin through Apoptosis and Membrane Disruption

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms23105500

    Recombinant scyreprocin (rScyreprocin) suppressed tumor growth in vivo. ( A ) Relative tumor volume (RTV) in different treatment groups. Cisplatin (CDDP, 3 mg kg −1 ), rScyreprocin (1.8 mg kg −1 ), and PBS (control) were given by intratumor injections; tumor volumes were measured every 3 days ( n = 6). ( B ) Body weight of mice in different treatment groups. The body weights of the mice were measured every 3 days ( n = 6). ( C ) Tumor tissues dissected from mice with different treatments. ( D ) Tumor weight of each group ( n = 6). ( E ) H E, TUNEL, Ki-67, and CD31 staining of tumor tissue sections obtained from mice with different treatments (scale bar = 50 μm). ( F ) Quantification of percent of Ki-67 + and CD31 + areas of each group ( n = 5). Data are presented as means ± standard deviation (SD). In ( A ), data were normalized to the initial tumor volume measured at day 0. In ( B ), data were normalized to the control group and analyzed by one-way ANOVA with Tukey post-tests (*** p
    Figure Legend Snippet: Recombinant scyreprocin (rScyreprocin) suppressed tumor growth in vivo. ( A ) Relative tumor volume (RTV) in different treatment groups. Cisplatin (CDDP, 3 mg kg −1 ), rScyreprocin (1.8 mg kg −1 ), and PBS (control) were given by intratumor injections; tumor volumes were measured every 3 days ( n = 6). ( B ) Body weight of mice in different treatment groups. The body weights of the mice were measured every 3 days ( n = 6). ( C ) Tumor tissues dissected from mice with different treatments. ( D ) Tumor weight of each group ( n = 6). ( E ) H E, TUNEL, Ki-67, and CD31 staining of tumor tissue sections obtained from mice with different treatments (scale bar = 50 μm). ( F ) Quantification of percent of Ki-67 + and CD31 + areas of each group ( n = 5). Data are presented as means ± standard deviation (SD). In ( A ), data were normalized to the initial tumor volume measured at day 0. In ( B ), data were normalized to the control group and analyzed by one-way ANOVA with Tukey post-tests (*** p

    Techniques Used: Recombinant, In Vivo, Mouse Assay, TUNEL Assay, Staining, Standard Deviation

    5) Product Images from "lncRNA MALAT1 binds chromatin remodeling subunit BRG1 to epigenetically promote inflammation-related hepatocellular carcinoma progression"

    Article Title: lncRNA MALAT1 binds chromatin remodeling subunit BRG1 to epigenetically promote inflammation-related hepatocellular carcinoma progression

    Journal: Oncoimmunology

    doi: 10.1080/2162402X.2018.1518628

    In vivo knockdown of MALAT1 in HCC tissues suppresses HCC growth. A) RT-qPCR analysis of MALAT1 expression in SMMC-LTNM tumor tissue two weeks after intratumoral injection of cholesterol-conjugated MALAT1 silence (mal_aso) or negative control (mal_nc). B, C) Two weeks after subcutaneous inoculation of SMMC-LTNM tumor cells, HCC-bearing nude mice were treated by intratumoral injection of mal_aso or mal_nc, respectively. Tumor volume B) and serum AFP levels C) were shown. D) H E staining and detection of Ki-67, MMP9, BCL2 and CD31 by IHC in HCC tissues was performed two weeks after intratumoral injection of cholesterol-conjugated mal_aso or mal_nc. IHC staining score were analyzed statistically (right panel). Scale bars = 50μm or 500μm. Data are shown as mean± s.e.m. (n = 3) (A, B, C and D). Data are shown one representative experiment (D) Similar results were obtained in three independent experiments. * P
    Figure Legend Snippet: In vivo knockdown of MALAT1 in HCC tissues suppresses HCC growth. A) RT-qPCR analysis of MALAT1 expression in SMMC-LTNM tumor tissue two weeks after intratumoral injection of cholesterol-conjugated MALAT1 silence (mal_aso) or negative control (mal_nc). B, C) Two weeks after subcutaneous inoculation of SMMC-LTNM tumor cells, HCC-bearing nude mice were treated by intratumoral injection of mal_aso or mal_nc, respectively. Tumor volume B) and serum AFP levels C) were shown. D) H E staining and detection of Ki-67, MMP9, BCL2 and CD31 by IHC in HCC tissues was performed two weeks after intratumoral injection of cholesterol-conjugated mal_aso or mal_nc. IHC staining score were analyzed statistically (right panel). Scale bars = 50μm or 500μm. Data are shown as mean± s.e.m. (n = 3) (A, B, C and D). Data are shown one representative experiment (D) Similar results were obtained in three independent experiments. * P

    Techniques Used: In Vivo, Quantitative RT-PCR, Expressing, Injection, Allele-specific Oligonucleotide, Negative Control, Mouse Assay, Staining, Immunohistochemistry

    6) Product Images from "Epigenetic dysregulation underpins tumorigenesis in a cutaneous tumor syndrome"

    Article Title: Epigenetic dysregulation underpins tumorigenesis in a cutaneous tumor syndrome

    Journal: bioRxiv

    doi: 10.1101/687459

    Intratumoral heterogeneity of DNMT3A mutation in CCS tumors. a , DNMT3A somatic mutation lollipop diagram for CCS tumors b , Spectrum of mutant variant allele fractions (VAF) of tumors in this study. c , Sampling of additional, deeper slices from a single tumor (PD40537a) reveals intratumoral heterogeneity of DNMT3A mutations (tumor indicated with grey sphere, intratumoral clones with coloured spheres). d , Geographic sampling of distinct histophenotypes (of cylindroma and spiradenoma) within a single tumor section (PD40542e) highlights marked clonal heterogeneity particularly of DNMT3A mutations. e , Protein expression of DNMT3A and Ki-67 is variable within a “cylinder” of CCS tumor and across cylinders (an adjacent outlined cylinder of cells showing of loss of DNMT3A expression).
    Figure Legend Snippet: Intratumoral heterogeneity of DNMT3A mutation in CCS tumors. a , DNMT3A somatic mutation lollipop diagram for CCS tumors b , Spectrum of mutant variant allele fractions (VAF) of tumors in this study. c , Sampling of additional, deeper slices from a single tumor (PD40537a) reveals intratumoral heterogeneity of DNMT3A mutations (tumor indicated with grey sphere, intratumoral clones with coloured spheres). d , Geographic sampling of distinct histophenotypes (of cylindroma and spiradenoma) within a single tumor section (PD40542e) highlights marked clonal heterogeneity particularly of DNMT3A mutations. e , Protein expression of DNMT3A and Ki-67 is variable within a “cylinder” of CCS tumor and across cylinders (an adjacent outlined cylinder of cells showing of loss of DNMT3A expression).

    Techniques Used: Mutagenesis, Variant Assay, Sampling, Clone Assay, Expressing

    7) Product Images from "Mechanism and Molecular Network of RBM8A-Mediated Regulation of Oxaliplatin Resistance in Hepatocellular Carcinoma"

    Article Title: Mechanism and Molecular Network of RBM8A-Mediated Regulation of Oxaliplatin Resistance in Hepatocellular Carcinoma

    Journal: Frontiers in Oncology

    doi: 10.3389/fonc.2020.585452

    Modulation of RBM8A expression affects proliferation, apoptosis and cell cycle progression in parental cell lines (PCLs) and drug-resistant (DR)-hepatocellular carcinoma (HCC) cells. (A) Cell proliferation measured using the Cell Counting Kit-8. * P
    Figure Legend Snippet: Modulation of RBM8A expression affects proliferation, apoptosis and cell cycle progression in parental cell lines (PCLs) and drug-resistant (DR)-hepatocellular carcinoma (HCC) cells. (A) Cell proliferation measured using the Cell Counting Kit-8. * P

    Techniques Used: Expressing, Cell Counting

    Involvement of the epithelial–mesenchymal transition (EMT) in RBM8A-mediated proliferation, invasion and drug resistance of hepatocellular carcinoma (HCC) cells. (A) Cell proliferation was analyzed in PCL-MHCC97H-NC, PCL-MHCC97H-RBM8A-OE, DR-MHCC97H-NC and DR-MHCC97H- RBM8A-OE cells in the presence or absence of the EMT inhibitor C19 using the CCK8 assay. (B) Wound-healing assay with or without EMT inhibitor C19. The scraped areas were photographed at 0 and 48 h after scraping. Migration efficiency was quantitated at 48 h after scraping (right). (C) Transwell analysis with or without EMT inhibitor C19. (D) Matrigel-Transwell analysis with or without EMT inhibitor C19. Magnification, 40×. Scale bar, 50 μm.
    Figure Legend Snippet: Involvement of the epithelial–mesenchymal transition (EMT) in RBM8A-mediated proliferation, invasion and drug resistance of hepatocellular carcinoma (HCC) cells. (A) Cell proliferation was analyzed in PCL-MHCC97H-NC, PCL-MHCC97H-RBM8A-OE, DR-MHCC97H-NC and DR-MHCC97H- RBM8A-OE cells in the presence or absence of the EMT inhibitor C19 using the CCK8 assay. (B) Wound-healing assay with or without EMT inhibitor C19. The scraped areas were photographed at 0 and 48 h after scraping. Migration efficiency was quantitated at 48 h after scraping (right). (C) Transwell analysis with or without EMT inhibitor C19. (D) Matrigel-Transwell analysis with or without EMT inhibitor C19. Magnification, 40×. Scale bar, 50 μm.

    Techniques Used: CCK-8 Assay, Wound Healing Assay, Migration

    8) Product Images from "Deregulating MYC in a model of HER2+ breast cancer mimics human intertumoral heterogeneity"

    Article Title: Deregulating MYC in a model of HER2+ breast cancer mimics human intertumoral heterogeneity

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI126390

    MYC phosphorylation is elevated in HER2 + patient tumors and correlated with HER2 expression. ( A ) Immunofluorescence images of 2 human HER2 + breast tumors from a TMA of 75 HER2 + patients with local disease showing CK19 (green) and p-S62-MYC (red) expression, with DAPI staining nuclei (blue); insets show higher magnification. Scale bars: 100 μm. ( B ) TMA tumor images were segmented for single cells and cells were classified as part of the tumor (CK19 + ) or nontumor stromal (CK19 – ) compartment. The frequency of p-S62-MYC positivity is compared between the compartments, with tumors arranged by the Z -score of frequency difference ( n = 71 assessable cores). SDs calculated from comparing frequencies between patient-matched cores (patients with one sample are grouped to right, arranged by p-S62-MYC frequency in tumor cells). ( C ) A patient-paired vertical scatterplot showing p-S62-MYC + cell frequency between the nontumor stroma and tumor compartments of patients ( n = 71). ( D ) Immunofluorescence images showing expression of CK19 (green), HER2 (red), and DAPI staining (blue) in patient tumors from A . Scale bars: 100 μm. ( E ) The frequency of p-S62-MYC + tumor cells is compared between the HER2 hi , HER2 med , and HER2 lo fractions of each tumor containing at least 2% HER2 hi/med tumor cells ( n = 67). Tumors are arranged by the cumulative Z -score of p-S62-MYC frequency between HER2 hi , HER2 med , and HER2 lo fractions. SDs shown between patient-matched cores (patients with one sample are grouped to right, arranged by the frequency of p-S62-MYC + cells in the HER2 hi fraction). ( F ) A patient-paired vertical scatterplot showing p-S62-MYC + cell frequency between the HER2 hi , HER2 med , and HER2 lo tumor cell fractions ( n = 67). ( G ) The frequency of Ki-67 + cells is compared between HER2 hi , HER2 med , and HER2 lo fractions as in F . ( H ) The frequency of Ki-67 + cells is shown between the p-S62-MYC–positive and –negative tumor fractions ( n = 71). **** P
    Figure Legend Snippet: MYC phosphorylation is elevated in HER2 + patient tumors and correlated with HER2 expression. ( A ) Immunofluorescence images of 2 human HER2 + breast tumors from a TMA of 75 HER2 + patients with local disease showing CK19 (green) and p-S62-MYC (red) expression, with DAPI staining nuclei (blue); insets show higher magnification. Scale bars: 100 μm. ( B ) TMA tumor images were segmented for single cells and cells were classified as part of the tumor (CK19 + ) or nontumor stromal (CK19 – ) compartment. The frequency of p-S62-MYC positivity is compared between the compartments, with tumors arranged by the Z -score of frequency difference ( n = 71 assessable cores). SDs calculated from comparing frequencies between patient-matched cores (patients with one sample are grouped to right, arranged by p-S62-MYC frequency in tumor cells). ( C ) A patient-paired vertical scatterplot showing p-S62-MYC + cell frequency between the nontumor stroma and tumor compartments of patients ( n = 71). ( D ) Immunofluorescence images showing expression of CK19 (green), HER2 (red), and DAPI staining (blue) in patient tumors from A . Scale bars: 100 μm. ( E ) The frequency of p-S62-MYC + tumor cells is compared between the HER2 hi , HER2 med , and HER2 lo fractions of each tumor containing at least 2% HER2 hi/med tumor cells ( n = 67). Tumors are arranged by the cumulative Z -score of p-S62-MYC frequency between HER2 hi , HER2 med , and HER2 lo fractions. SDs shown between patient-matched cores (patients with one sample are grouped to right, arranged by the frequency of p-S62-MYC + cells in the HER2 hi fraction). ( F ) A patient-paired vertical scatterplot showing p-S62-MYC + cell frequency between the HER2 hi , HER2 med , and HER2 lo tumor cell fractions ( n = 67). ( G ) The frequency of Ki-67 + cells is compared between HER2 hi , HER2 med , and HER2 lo fractions as in F . ( H ) The frequency of Ki-67 + cells is shown between the p-S62-MYC–positive and –negative tumor fractions ( n = 71). **** P

    Techniques Used: Expressing, Immunofluorescence, Staining

    9) Product Images from "Deregulating MYC in a model of HER2+ breast cancer mimics human intertumoral heterogeneity"

    Article Title: Deregulating MYC in a model of HER2+ breast cancer mimics human intertumoral heterogeneity

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI126390

    MYC phosphorylation is elevated in HER2 + patient tumors and correlated with HER2 expression. ( A ) Immunofluorescence images of 2 human HER2 + breast tumors from a TMA of 75 HER2 + patients with local disease showing CK19 (green) and p-S62-MYC (red) expression, with DAPI staining nuclei (blue); insets show higher magnification. Scale bars: 100 μm. ( B ) TMA tumor images were segmented for single cells and cells were classified as part of the tumor (CK19 + ) or nontumor stromal (CK19 – ) compartment. The frequency of p-S62-MYC positivity is compared between the compartments, with tumors arranged by the Z -score of frequency difference ( n = 71 assessable cores). SDs calculated from comparing frequencies between patient-matched cores (patients with one sample are grouped to right, arranged by p-S62-MYC frequency in tumor cells). ( C ) A patient-paired vertical scatterplot showing p-S62-MYC + cell frequency between the nontumor stroma and tumor compartments of patients ( n = 71). ( D ) Immunofluorescence images showing expression of CK19 (green), HER2 (red), and DAPI staining (blue) in patient tumors from A . Scale bars: 100 μm. ( E ) The frequency of p-S62-MYC + tumor cells is compared between the HER2 hi , HER2 med , and HER2 lo fractions of each tumor containing at least 2% HER2 hi/med tumor cells ( n = 67). Tumors are arranged by the cumulative Z -score of p-S62-MYC frequency between HER2 hi , HER2 med , and HER2 lo fractions. SDs shown between patient-matched cores (patients with one sample are grouped to right, arranged by the frequency of p-S62-MYC + cells in the HER2 hi fraction). ( F ) A patient-paired vertical scatterplot showing p-S62-MYC + cell frequency between the HER2 hi , HER2 med , and HER2 lo tumor cell fractions ( n = 67). ( G ) The frequency of Ki-67 + cells is compared between HER2 hi , HER2 med , and HER2 lo fractions as in F . ( H ) The frequency of Ki-67 + cells is shown between the p-S62-MYC–positive and –negative tumor fractions ( n = 71). **** P
    Figure Legend Snippet: MYC phosphorylation is elevated in HER2 + patient tumors and correlated with HER2 expression. ( A ) Immunofluorescence images of 2 human HER2 + breast tumors from a TMA of 75 HER2 + patients with local disease showing CK19 (green) and p-S62-MYC (red) expression, with DAPI staining nuclei (blue); insets show higher magnification. Scale bars: 100 μm. ( B ) TMA tumor images were segmented for single cells and cells were classified as part of the tumor (CK19 + ) or nontumor stromal (CK19 – ) compartment. The frequency of p-S62-MYC positivity is compared between the compartments, with tumors arranged by the Z -score of frequency difference ( n = 71 assessable cores). SDs calculated from comparing frequencies between patient-matched cores (patients with one sample are grouped to right, arranged by p-S62-MYC frequency in tumor cells). ( C ) A patient-paired vertical scatterplot showing p-S62-MYC + cell frequency between the nontumor stroma and tumor compartments of patients ( n = 71). ( D ) Immunofluorescence images showing expression of CK19 (green), HER2 (red), and DAPI staining (blue) in patient tumors from A . Scale bars: 100 μm. ( E ) The frequency of p-S62-MYC + tumor cells is compared between the HER2 hi , HER2 med , and HER2 lo fractions of each tumor containing at least 2% HER2 hi/med tumor cells ( n = 67). Tumors are arranged by the cumulative Z -score of p-S62-MYC frequency between HER2 hi , HER2 med , and HER2 lo fractions. SDs shown between patient-matched cores (patients with one sample are grouped to right, arranged by the frequency of p-S62-MYC + cells in the HER2 hi fraction). ( F ) A patient-paired vertical scatterplot showing p-S62-MYC + cell frequency between the HER2 hi , HER2 med , and HER2 lo tumor cell fractions ( n = 67). ( G ) The frequency of Ki-67 + cells is compared between HER2 hi , HER2 med , and HER2 lo fractions as in F . ( H ) The frequency of Ki-67 + cells is shown between the p-S62-MYC–positive and –negative tumor fractions ( n = 71). **** P

    Techniques Used: Expressing, Immunofluorescence, Staining

    10) Product Images from "High expression of 14-3-3ơ indicates poor prognosis and progression of lung adenocarcinoma"

    Article Title: High expression of 14-3-3ơ indicates poor prognosis and progression of lung adenocarcinoma

    Journal: Oncology Letters

    doi: 10.3892/ol.2022.13323

    Overexpression of 14-3-3ơ promotes the growth of LUAD cells. (A) 14-3-3ơ was overexpressed in NCI-H1299 LUAD cells by targeted plasmids. (B) Overexpression 14-3-3ơ significantly stimulated cell proliferation in NCI-H1299 cells. Cell viability was detected with an ATP-lite assay. (C) Overexpression 14-3-3ơ significantly promoted cell colony formation by NCI-H1299 cells. (D) The anchorage-independent growth of NCI-H1299 cells in a soft agar assay was increased upon 14-3-3σ overexpression (scale bar, 100 µm). ns, no significance; **P
    Figure Legend Snippet: Overexpression of 14-3-3ơ promotes the growth of LUAD cells. (A) 14-3-3ơ was overexpressed in NCI-H1299 LUAD cells by targeted plasmids. (B) Overexpression 14-3-3ơ significantly stimulated cell proliferation in NCI-H1299 cells. Cell viability was detected with an ATP-lite assay. (C) Overexpression 14-3-3ơ significantly promoted cell colony formation by NCI-H1299 cells. (D) The anchorage-independent growth of NCI-H1299 cells in a soft agar assay was increased upon 14-3-3σ overexpression (scale bar, 100 µm). ns, no significance; **P

    Techniques Used: Over Expression, Soft Agar Assay

    14-3-3σ silencing inhibits LUAD cell growth by inducing apoptosis. (A) 14-3-3ơ was knockdown in A-549 LUAD cells by targeted siRNA. (B) 14-3-3ơ silencing significantly suppressed cell proliferation in A-549 cells. Cell viability was detected with an ATP-lite assay. (C) 14-3-3ơ silencing significantly suppressed colony formation by A-549 cells. (D) 14-3-3σ depletion induced apoptosis by increasing PARP and C-Caspase-3. A-549 LUAD cells were transfected siRNAs targeting 14-3-3σ, followed by western blot analysis. (E) The anchorage-independent growth of A-549 cells sd measured by a soft agar assay was reduced upon 14-3-3σ silencing (scale bar, 100 µm). ns, no significance; **P
    Figure Legend Snippet: 14-3-3σ silencing inhibits LUAD cell growth by inducing apoptosis. (A) 14-3-3ơ was knockdown in A-549 LUAD cells by targeted siRNA. (B) 14-3-3ơ silencing significantly suppressed cell proliferation in A-549 cells. Cell viability was detected with an ATP-lite assay. (C) 14-3-3ơ silencing significantly suppressed colony formation by A-549 cells. (D) 14-3-3σ depletion induced apoptosis by increasing PARP and C-Caspase-3. A-549 LUAD cells were transfected siRNAs targeting 14-3-3σ, followed by western blot analysis. (E) The anchorage-independent growth of A-549 cells sd measured by a soft agar assay was reduced upon 14-3-3σ silencing (scale bar, 100 µm). ns, no significance; **P

    Techniques Used: Transfection, Western Blot, Soft Agar Assay

    11) Product Images from "Mesenchymal stem cells-derived small extracellular vesicles alleviate diabetic retinopathy by delivering NEDD4"

    Article Title: Mesenchymal stem cells-derived small extracellular vesicles alleviate diabetic retinopathy by delivering NEDD4

    Journal: Stem Cell Research & Therapy

    doi: 10.1186/s13287-022-02983-0

    AKT inhibition impaired MSC-sEV-induced therapeutic effects in vitro. A Western blot analysis for the expressions of NRF2 and p-AKT in RPE cells treated with LY294002. B Immunofluorescence staining of NRF2 in RPE cells treated with LY294002. Scale bars, 25 μm. C Detection of ROS generation in RPE cells treated with LY294002. Scale bars, 100 μm. D CCK8 assay for the proliferation ability of RPE cells treated with LY294002 ( n = 4). E Western blot analysis for the expressions of PCNA, Bcl-2 and Bax in RPE cells treated with LY294002. F Representative immunofluorescence staining images of Ki-67 in RPE cells treated with LY294002. Scale bars, 25 μm. All data are presented as means ± SEM. ns, not significant, * P
    Figure Legend Snippet: AKT inhibition impaired MSC-sEV-induced therapeutic effects in vitro. A Western blot analysis for the expressions of NRF2 and p-AKT in RPE cells treated with LY294002. B Immunofluorescence staining of NRF2 in RPE cells treated with LY294002. Scale bars, 25 μm. C Detection of ROS generation in RPE cells treated with LY294002. Scale bars, 100 μm. D CCK8 assay for the proliferation ability of RPE cells treated with LY294002 ( n = 4). E Western blot analysis for the expressions of PCNA, Bcl-2 and Bax in RPE cells treated with LY294002. F Representative immunofluorescence staining images of Ki-67 in RPE cells treated with LY294002. Scale bars, 25 μm. All data are presented as means ± SEM. ns, not significant, * P

    Techniques Used: Inhibition, In Vitro, Western Blot, Immunofluorescence, Staining, CCK-8 Assay

    Proposed model for the therapeutic roles of MSC-sEV in DR. MSC-sEV-delivered NEDD4 mediates the ubiquitination and degradation of PTEN, thus promoting the activation of AKT signaling pathway and upregulating NRF2 expression to alleviate the oxidative damage and apoptosis of RPE cells
    Figure Legend Snippet: Proposed model for the therapeutic roles of MSC-sEV in DR. MSC-sEV-delivered NEDD4 mediates the ubiquitination and degradation of PTEN, thus promoting the activation of AKT signaling pathway and upregulating NRF2 expression to alleviate the oxidative damage and apoptosis of RPE cells

    Techniques Used: Activation Assay, Expressing

    Retinal therapeutic effects of MSC-sEV on diabetic rats. A Representative retinal H E staining images after treatment. Scale bars, 100 μm. B Retinal thickness analysis of each group ( n = 6). C Representative images of immunohistochemistry staining of cleaved caspase-3. Scale bars, 100 μm. D Western blot analysis for the retinal expression of PCNA, Bcl-2 and Bax. E Retinal MDA and SOD levels measurement ( n = 3). F Representative images of retinal immunohistochemistry staining of NRF2. Scale bars, 100 μm. G QRT-PCR for the relative mRNA levels of NRF2-related genes ( n = 3). H Western blot analysis for the retinal expression of GPX1, NQO1, HO-1 and NRF2. All data are presented as means ± SEM. ns, not significant, * P
    Figure Legend Snippet: Retinal therapeutic effects of MSC-sEV on diabetic rats. A Representative retinal H E staining images after treatment. Scale bars, 100 μm. B Retinal thickness analysis of each group ( n = 6). C Representative images of immunohistochemistry staining of cleaved caspase-3. Scale bars, 100 μm. D Western blot analysis for the retinal expression of PCNA, Bcl-2 and Bax. E Retinal MDA and SOD levels measurement ( n = 3). F Representative images of retinal immunohistochemistry staining of NRF2. Scale bars, 100 μm. G QRT-PCR for the relative mRNA levels of NRF2-related genes ( n = 3). H Western blot analysis for the retinal expression of GPX1, NQO1, HO-1 and NRF2. All data are presented as means ± SEM. ns, not significant, * P

    Techniques Used: Staining, Immunohistochemistry, Western Blot, Expressing, Multiple Displacement Amplification, Quantitative RT-PCR

    MSC-sEV exerted repairing effects through PTEN/AKT signaling pathway. A Western blot analysis for the expressions of cell signaling pathway in RPE cells after treatment. B Immunofluorescence staining of PTEN and p-AKT in RPE cells after treatment. Scale bars, 25 μm. C Representative immunohistochemistry staining images of PTEN and p-AKT in retinal tissues. Scale bars, 100 μm. D Western blot analysis for the expressions of PTEN and p-AKT in retinal tissues. E Western blot analysis for the expressions of PTEN, p-AKT and NRF2 in RPE cells transfected with PTEN siRNA. F Representative immunofluorescence staining images of NRF2 in RPE cells transfected with PTEN siRNA. Scale bars, 25 μm. G Detection of ROS generation in RPE cells transfected with PTEN siRNA. Scale bars, 100 μm. H CCK8 assay for the proliferation ability of RPE cells transfected with PTEN siRNA ( n = 4). I Western blot analysis for the expressions of PCNA, Bcl-2 and Bax in RPE cells transfected with PTEN siRNA. All data are presented as means ± SEM. ns, not significant, * P
    Figure Legend Snippet: MSC-sEV exerted repairing effects through PTEN/AKT signaling pathway. A Western blot analysis for the expressions of cell signaling pathway in RPE cells after treatment. B Immunofluorescence staining of PTEN and p-AKT in RPE cells after treatment. Scale bars, 25 μm. C Representative immunohistochemistry staining images of PTEN and p-AKT in retinal tissues. Scale bars, 100 μm. D Western blot analysis for the expressions of PTEN and p-AKT in retinal tissues. E Western blot analysis for the expressions of PTEN, p-AKT and NRF2 in RPE cells transfected with PTEN siRNA. F Representative immunofluorescence staining images of NRF2 in RPE cells transfected with PTEN siRNA. Scale bars, 25 μm. G Detection of ROS generation in RPE cells transfected with PTEN siRNA. Scale bars, 100 μm. H CCK8 assay for the proliferation ability of RPE cells transfected with PTEN siRNA ( n = 4). I Western blot analysis for the expressions of PCNA, Bcl-2 and Bax in RPE cells transfected with PTEN siRNA. All data are presented as means ± SEM. ns, not significant, * P

    Techniques Used: Western Blot, Immunofluorescence, Staining, Immunohistochemistry, Transfection, CCK-8 Assay

    MSC-sEV protected RPE cells against HG conditions in vitro. A The internalization of PKH-26-labeled MSC-sEV by RPE cells was detected by a confocal microscope. Scale bars, 25 μm. B Immunofluorescence analysis of Ki-67 in RPE cells. Scale bars, 25 μm. C CCK8 assay for the proliferation ability of RPE cells ( n = 4). D Western blot analysis for the expressions of PCNA, Bcl-2 and Bax in RPE cells. E Detection of ROS generation in RPE cells. Scale bars, 100 μm. F MDA and SOD level measurement in RPE cells ( n = 3). G Western blot analysis for the expressions of GPX1, NQO1, HO-1 and NRF2 in RPE cells. H Immunofluorescence staining of NRF2 in RPE cells. Scale bars, 25 μm. All data are presented as means ± SEM. ns, not significant, * P
    Figure Legend Snippet: MSC-sEV protected RPE cells against HG conditions in vitro. A The internalization of PKH-26-labeled MSC-sEV by RPE cells was detected by a confocal microscope. Scale bars, 25 μm. B Immunofluorescence analysis of Ki-67 in RPE cells. Scale bars, 25 μm. C CCK8 assay for the proliferation ability of RPE cells ( n = 4). D Western blot analysis for the expressions of PCNA, Bcl-2 and Bax in RPE cells. E Detection of ROS generation in RPE cells. Scale bars, 100 μm. F MDA and SOD level measurement in RPE cells ( n = 3). G Western blot analysis for the expressions of GPX1, NQO1, HO-1 and NRF2 in RPE cells. H Immunofluorescence staining of NRF2 in RPE cells. Scale bars, 25 μm. All data are presented as means ± SEM. ns, not significant, * P

    Techniques Used: In Vitro, Labeling, Microscopy, Immunofluorescence, CCK-8 Assay, Western Blot, Multiple Displacement Amplification, Staining

    12) Product Images from "The role of NLRP3 inflammasome in 5-fluorouracil resistance of oral squamous cell carcinoma"

    Article Title: The role of NLRP3 inflammasome in 5-fluorouracil resistance of oral squamous cell carcinoma

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    doi: 10.1186/s13046-017-0553-x

    NLRP3 inflammasome expression is increased in OSCC tissues. a mRNA expression of NLRP3, Caspase1 and pro-IL-1β in 21 paired OSCC and adjacent normal tissues was determined by real-time qPCR. b Protein expression of NLRP3, Caspase1 and IL-1β in 21 paired OSCC and adjacent normal tissues by western blot. c Immunohistochemical staining for NLRP3 and Ki-67. (magnification 100× for NLRP3 staining and 200× for Ki-67 staining)
    Figure Legend Snippet: NLRP3 inflammasome expression is increased in OSCC tissues. a mRNA expression of NLRP3, Caspase1 and pro-IL-1β in 21 paired OSCC and adjacent normal tissues was determined by real-time qPCR. b Protein expression of NLRP3, Caspase1 and IL-1β in 21 paired OSCC and adjacent normal tissues by western blot. c Immunohistochemical staining for NLRP3 and Ki-67. (magnification 100× for NLRP3 staining and 200× for Ki-67 staining)

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Western Blot, Immunohistochemistry, Staining

    Kaplan–Meier with log rank test analysis of the OS and DFS rates for 103 OSCC patients. The influence of NLRP3 expression on OS ( a ) and DFS ( b ) of OSCC patients. Combined assessment of the influence of NLRP3 and Ki-67 expression on OS ( c ) and DFS ( d ) of OSCC patients
    Figure Legend Snippet: Kaplan–Meier with log rank test analysis of the OS and DFS rates for 103 OSCC patients. The influence of NLRP3 expression on OS ( a ) and DFS ( b ) of OSCC patients. Combined assessment of the influence of NLRP3 and Ki-67 expression on OS ( c ) and DFS ( d ) of OSCC patients

    Techniques Used: Expressing

    13) Product Images from "The COX10-AS1/miR-641/E2F6 Feedback Loop Is Involved in the Progression of Glioma"

    Article Title: The COX10-AS1/miR-641/E2F6 Feedback Loop Is Involved in the Progression of Glioma

    Journal: Frontiers in Oncology

    doi: 10.3389/fonc.2021.648152

    COX10-AS1 promotes glioma growth in vivo . (A, B) The bioluminescent images of the tumours formed in the brains of nude mice were acquired at days 1, 10 and 20 after implantation. (C) Overall survival was compared between the sh-COX10-AS1 and sh-NC groups by Kaplan-Meier survival curves. (D) Immunohistochemistry for Ki-67 in the sh-COX10-AS1 and sh-NC groups. (E) TUNEL staining in the sh-COX10-AS1 and sh-NC groups. **P
    Figure Legend Snippet: COX10-AS1 promotes glioma growth in vivo . (A, B) The bioluminescent images of the tumours formed in the brains of nude mice were acquired at days 1, 10 and 20 after implantation. (C) Overall survival was compared between the sh-COX10-AS1 and sh-NC groups by Kaplan-Meier survival curves. (D) Immunohistochemistry for Ki-67 in the sh-COX10-AS1 and sh-NC groups. (E) TUNEL staining in the sh-COX10-AS1 and sh-NC groups. **P

    Techniques Used: In Vivo, Mouse Assay, Immunohistochemistry, TUNEL Assay, Staining

    E2F6 promotes glioma growth in vivo . (A, B) The bioluminescent images of the tumours formed in the brains of nude mice were acquired at days 1, 10 and 20 after implantation. (C) Overall survival was compared between the sh-E2F6 and sh-NC groups by Kaplan-Meier survival curves. (D) Immunohistochemistry for Ki-67 in the sh-E2F6 and sh-NC groups. (E) Immunohistochemistry for TUNEL staining in the sh-E2F6 and sh-NC groups.
    Figure Legend Snippet: E2F6 promotes glioma growth in vivo . (A, B) The bioluminescent images of the tumours formed in the brains of nude mice were acquired at days 1, 10 and 20 after implantation. (C) Overall survival was compared between the sh-E2F6 and sh-NC groups by Kaplan-Meier survival curves. (D) Immunohistochemistry for Ki-67 in the sh-E2F6 and sh-NC groups. (E) Immunohistochemistry for TUNEL staining in the sh-E2F6 and sh-NC groups.

    Techniques Used: In Vivo, Mouse Assay, Immunohistochemistry, TUNEL Assay, Staining

    14) Product Images from "CLDN8 promotes colorectal cancer cell proliferation, migration, and invasion by activating MAPK/ERK signaling"

    Article Title: CLDN8 promotes colorectal cancer cell proliferation, migration, and invasion by activating MAPK/ERK signaling

    Journal: Cancer Management and Research

    doi: 10.2147/CMAR.S189558

    Knockdown of CLDN8 expression inhibits CRC growth in nude mice. Notes: ( A, B ) CLDN8 knockdown markedly reduced tumor weight in vivo. ( C , E ) IHC staining confirmed the knockdown expression of CLDN8 in SW480 and HT-29–induced tumor. ( D , F ) IHC staining showed that tumors formed by CLDN8-knockdown cells exhibited lower positive percentage of Ki-67 than control tumors. ( G ) Quantitative analysis of IHC staining in SW480-induced tumor. ( H ) Quantitative analysis of IHC staining in HT-29–induced tumor. The meaning of each group name: Knock-NC, the negative control group of TROP2 knockdown; CLDN8-knock, knockdown of CLDN8. * P
    Figure Legend Snippet: Knockdown of CLDN8 expression inhibits CRC growth in nude mice. Notes: ( A, B ) CLDN8 knockdown markedly reduced tumor weight in vivo. ( C , E ) IHC staining confirmed the knockdown expression of CLDN8 in SW480 and HT-29–induced tumor. ( D , F ) IHC staining showed that tumors formed by CLDN8-knockdown cells exhibited lower positive percentage of Ki-67 than control tumors. ( G ) Quantitative analysis of IHC staining in SW480-induced tumor. ( H ) Quantitative analysis of IHC staining in HT-29–induced tumor. The meaning of each group name: Knock-NC, the negative control group of TROP2 knockdown; CLDN8-knock, knockdown of CLDN8. * P

    Techniques Used: Expressing, Mouse Assay, In Vivo, Immunohistochemistry, Staining, Negative Control

    Effects of CLDN8 on CRC cell proliferation migration and invasion. Notes: ( A, B ) Western blot analysis confirmed the successful transfection and stable establishment in both SW480 and HT-29 cells. ( C ) The results of CCK-8 assay revealed that CLDN8 overexpression promoted the proliferation of SW480 and HT-29 cells, while CLDN8 knockdown significantly decreased the proliferation rate in a time-dependent manner. ( D, E ) The results of Transwell invasion assay showed that upregulation of CLDN8 expression in SW480 and HT-29 cells significantly enhanced cell invasion, which was inhibited by CLDN8 knockdown. ( F – H ) Wound healing assay showed that CLDN8 overexpression promoted SW480 and HT-29 cells migration, whereas downregulation of CLDN8 markedly reduced cell migration. The meaning of each group name: CLDN8-NC, the negative control group of CLDN8 overexpression; CLDN8, overexpression of CLDN8; Knock-NC, the negative control group of TROP2 knockdown; Knock, knockdown of CLDN8. * P
    Figure Legend Snippet: Effects of CLDN8 on CRC cell proliferation migration and invasion. Notes: ( A, B ) Western blot analysis confirmed the successful transfection and stable establishment in both SW480 and HT-29 cells. ( C ) The results of CCK-8 assay revealed that CLDN8 overexpression promoted the proliferation of SW480 and HT-29 cells, while CLDN8 knockdown significantly decreased the proliferation rate in a time-dependent manner. ( D, E ) The results of Transwell invasion assay showed that upregulation of CLDN8 expression in SW480 and HT-29 cells significantly enhanced cell invasion, which was inhibited by CLDN8 knockdown. ( F – H ) Wound healing assay showed that CLDN8 overexpression promoted SW480 and HT-29 cells migration, whereas downregulation of CLDN8 markedly reduced cell migration. The meaning of each group name: CLDN8-NC, the negative control group of CLDN8 overexpression; CLDN8, overexpression of CLDN8; Knock-NC, the negative control group of TROP2 knockdown; Knock, knockdown of CLDN8. * P

    Techniques Used: Migration, Western Blot, Transfection, CCK-8 Assay, Over Expression, Transwell Invasion Assay, Expressing, Wound Healing Assay, Negative Control

    15) Product Images from "AKR1C2 acts as a targetable oncogene in esophageal squamous cell carcinoma via activating PI3K/AKT signaling pathway, et al. AKR1C2 acts as a targetable oncogene in esophageal squamous cell carcinoma via activating PI3K/AKT signaling pathway"

    Article Title: AKR1C2 acts as a targetable oncogene in esophageal squamous cell carcinoma via activating PI3K/AKT signaling pathway, et al. AKR1C2 acts as a targetable oncogene in esophageal squamous cell carcinoma via activating PI3K/AKT signaling pathway

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.15604

    PI3K/AKT signalling pathway was regulated by AKR1C2. A, Three pairs of matched tumour/normal tissues were performed with RNA‐sequencing and the KEGG results were shown, and the PI3K/AKT signalling pathway was circled with a rectangle. B, The pAKT protein level was detected by Western blotting in six pairs of ESCC tissues and corresponding adjacent normal tissues. C, The KYSE30 cell was transfected with an empty vector or AKR1C2 plasmid for 72 h, mRNA sequencing analysis was performed, and the KEGG results were shown, the PI3K/AKT signalling pathway and platinum drug resistance were highlighted by rectangles. D, Western blotting analysis the change of pAKT in the indicated ESCC cell lines. E, The IHC was performed to detect the AKR1C2‐mediated expression change of pAKT and Ki‐67 in the excised tumours from tumour growth models. The arrows indicated regional areas, suggesting a positive correlation between the AKR1C2, pAKT and Ki‐67. The pictures were taken at 200× original magnification. Scale bar, 50 μm. F, The correlation between AKR1C2 and pAKT expression was analysed by IHC in 47 ESCC clinical samples ( r = .5669, P
    Figure Legend Snippet: PI3K/AKT signalling pathway was regulated by AKR1C2. A, Three pairs of matched tumour/normal tissues were performed with RNA‐sequencing and the KEGG results were shown, and the PI3K/AKT signalling pathway was circled with a rectangle. B, The pAKT protein level was detected by Western blotting in six pairs of ESCC tissues and corresponding adjacent normal tissues. C, The KYSE30 cell was transfected with an empty vector or AKR1C2 plasmid for 72 h, mRNA sequencing analysis was performed, and the KEGG results were shown, the PI3K/AKT signalling pathway and platinum drug resistance were highlighted by rectangles. D, Western blotting analysis the change of pAKT in the indicated ESCC cell lines. E, The IHC was performed to detect the AKR1C2‐mediated expression change of pAKT and Ki‐67 in the excised tumours from tumour growth models. The arrows indicated regional areas, suggesting a positive correlation between the AKR1C2, pAKT and Ki‐67. The pictures were taken at 200× original magnification. Scale bar, 50 μm. F, The correlation between AKR1C2 and pAKT expression was analysed by IHC in 47 ESCC clinical samples ( r = .5669, P

    Techniques Used: RNA Sequencing Assay, Western Blot, Transfection, Plasmid Preparation, Sequencing, Immunohistochemistry, Expressing

    16) Product Images from "R406 elicits anti-Warburg effect via Syk-dependent and -independent mechanisms to trigger apoptosis in glioma stem cells"

    Article Title: R406 elicits anti-Warburg effect via Syk-dependent and -independent mechanisms to trigger apoptosis in glioma stem cells

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-019-1587-0

    R406 synergistically enhances TMZ cytotoxicity against GSCs in vitro and in vivo. a Cell viability of GSCs after treatment with either R406 alone, TMZ alone or combination of two agents was measured using Muse cell analyzer. Quantification analysis demonstrated that combination of R406 and TMZ was superior to monotherapy with the single agent. b Combination of R406 and TMZ significantly delayed subcutaneous tumor growth in vivo compared to monotherapy. c IHC for tumor sections demonstrated that addition of R406 to TMZ decreased the numbers of proliferative cells, which were positive for Ki-67 (white arrow). d Protein was extracted from xenograft specimens and allocated for Western blot. Enhanced activation of caspase 3 was found in mice treated with combination of R406 and TMZ. e R406 plus TMZ significantly prolonged the survival of mice in the orthotopic model compared to monotherapy either with R406 or TMZ alone. ( NS not significant; * p
    Figure Legend Snippet: R406 synergistically enhances TMZ cytotoxicity against GSCs in vitro and in vivo. a Cell viability of GSCs after treatment with either R406 alone, TMZ alone or combination of two agents was measured using Muse cell analyzer. Quantification analysis demonstrated that combination of R406 and TMZ was superior to monotherapy with the single agent. b Combination of R406 and TMZ significantly delayed subcutaneous tumor growth in vivo compared to monotherapy. c IHC for tumor sections demonstrated that addition of R406 to TMZ decreased the numbers of proliferative cells, which were positive for Ki-67 (white arrow). d Protein was extracted from xenograft specimens and allocated for Western blot. Enhanced activation of caspase 3 was found in mice treated with combination of R406 and TMZ. e R406 plus TMZ significantly prolonged the survival of mice in the orthotopic model compared to monotherapy either with R406 or TMZ alone. ( NS not significant; * p

    Techniques Used: In Vitro, In Vivo, Immunohistochemistry, Western Blot, Activation Assay, Mouse Assay

    17) Product Images from "Long Noncoding RNA HEIH Promotes Colorectal Cancer Tumorigenesis via Counteracting miR-939‒Mediated Transcriptional Repression of Bcl-xL"

    Article Title: Long Noncoding RNA HEIH Promotes Colorectal Cancer Tumorigenesis via Counteracting miR-939‒Mediated Transcriptional Repression of Bcl-xL

    Journal: Cancer Research and Treatment : Official Journal of Korean Cancer Association

    doi: 10.4143/crt.2017.226

    The mutation of miR-939 binding sites on long noncoding RNA HEIH (lncRNA-HEIH) abolished the effects of lncRNA-HEIH on colorectal cancer tumorigenesis. (A) The expression of lncRNA-HEIH in lncRNA-HEIH or lncRNA-HEIH-mut stably overexpressed and control HT-29 cells was detected by quantitative real-time polymerase chain reaction and normalized to glyceraldehyde 3-phosphate dehydrogenase. (B) Cell proliferation rate of lncRNA-HEIH or lncRNA-HEIH-mut stably overexpressed and control HT-29 cells were detected by the Cell Counting Kit-8 assays. (C) Proliferative cells of lncRNA-HEIH or lncRNA-HEIH-mut stably overexpressed and control HT-29 were labeled with ethynyl deoxyuridine (EdU). Red color indicts EdU-positive cells. Scale bars=100 μm. (D) The level of apoptosis in lncRNA-HEIH or lncRNA-HEIH-mut stably overexpressed and control HT-29 cells was detected by TdT-mediated dUTP nick end labeling (TUNEL) staining. Blue color indicts TUNEL-positive cells. Scale bars=100 μm. For A-D, results are shown as mean±standard deviation (SD) from three independent experiments. **p
    Figure Legend Snippet: The mutation of miR-939 binding sites on long noncoding RNA HEIH (lncRNA-HEIH) abolished the effects of lncRNA-HEIH on colorectal cancer tumorigenesis. (A) The expression of lncRNA-HEIH in lncRNA-HEIH or lncRNA-HEIH-mut stably overexpressed and control HT-29 cells was detected by quantitative real-time polymerase chain reaction and normalized to glyceraldehyde 3-phosphate dehydrogenase. (B) Cell proliferation rate of lncRNA-HEIH or lncRNA-HEIH-mut stably overexpressed and control HT-29 cells were detected by the Cell Counting Kit-8 assays. (C) Proliferative cells of lncRNA-HEIH or lncRNA-HEIH-mut stably overexpressed and control HT-29 were labeled with ethynyl deoxyuridine (EdU). Red color indicts EdU-positive cells. Scale bars=100 μm. (D) The level of apoptosis in lncRNA-HEIH or lncRNA-HEIH-mut stably overexpressed and control HT-29 cells was detected by TdT-mediated dUTP nick end labeling (TUNEL) staining. Blue color indicts TUNEL-positive cells. Scale bars=100 μm. For A-D, results are shown as mean±standard deviation (SD) from three independent experiments. **p

    Techniques Used: Mutagenesis, Binding Assay, Expressing, Stable Transfection, Real-time Polymerase Chain Reaction, Cell Counting, Labeling, End Labeling, TUNEL Assay, Staining, Standard Deviation

    Knockdown of long noncoding RNA HEIH (lncRNA-HEIH) inhibits colorectal cancer tumorigenesis. (A) The expression of lncRNA-HEIH in lncRNA-HEIH stably knocked-down and control LoVo cells was detected by quantitative real-time polymerase chain reaction and normalized to glyceraldehyde 3-phosphate dehydrogenase. (B) Cell proliferation rate of lncRNA-HEIH stably knocked-down and control LoVo cells were detected by the Cell Counting Kit-8 assays. (C) Proliferative cells of lncRNA-HEIH stably knocked-down and control LoVo were labeled with ethynyl deoxyuridine (EdU). Red color indicts EdU-positive cells. Scale bars=100 μm. (D) The level of apoptosis in lncRNA-HEIH stably knocked-down and control LoVo cells was detected by TdT-mediated dUTP nick end labeling (TUNEL) staining. Blue color indicts TUNEL-positive cells. Scale bars=100 μm. For A-D, results are shown as mean±standard deviation (SD) from three independent experiments. *p
    Figure Legend Snippet: Knockdown of long noncoding RNA HEIH (lncRNA-HEIH) inhibits colorectal cancer tumorigenesis. (A) The expression of lncRNA-HEIH in lncRNA-HEIH stably knocked-down and control LoVo cells was detected by quantitative real-time polymerase chain reaction and normalized to glyceraldehyde 3-phosphate dehydrogenase. (B) Cell proliferation rate of lncRNA-HEIH stably knocked-down and control LoVo cells were detected by the Cell Counting Kit-8 assays. (C) Proliferative cells of lncRNA-HEIH stably knocked-down and control LoVo were labeled with ethynyl deoxyuridine (EdU). Red color indicts EdU-positive cells. Scale bars=100 μm. (D) The level of apoptosis in lncRNA-HEIH stably knocked-down and control LoVo cells was detected by TdT-mediated dUTP nick end labeling (TUNEL) staining. Blue color indicts TUNEL-positive cells. Scale bars=100 μm. For A-D, results are shown as mean±standard deviation (SD) from three independent experiments. *p

    Techniques Used: Expressing, Stable Transfection, Real-time Polymerase Chain Reaction, Cell Counting, Labeling, End Labeling, TUNEL Assay, Staining, Standard Deviation

    Enhanced expression of long noncoding RNA HEIH (lncRNA-HEIH) promotes colorectal cancer tumorigenesis. (A) The expression of lncRNA-HEIH in lncRNA-HEIH stably overexpressed and control HT-29 cells was detected by quantitative real-time polymerase chain reaction and normalized to glyceraldehyde 3-phosphat e dehydrogenase. (B) Cell proliferation rate of lncRNA-HEIH stably overexpressed and control HT-29 cells were detected by the Cell Counting Kit-8 assays. (C) Proliferative cells of lncRNA-HEIH stably overexpressed and control HT-29 were labeled with ethynyl deoxyuridine (EdU). Red color indicts EdU-positive cells. Scale bars=100 μm. (D) The level of apoptosis in lncRNA-HEIH stably overexpressed and control HT-29 cells was detected by TdT-mediated dUTP nick end labeling (TUNEL) staining. Blue color indicts TUNEL-positive cells. Scale bars=100 μm. For A-D, results are shown as mean±standard deviation (SD). from three independent experiments. **p
    Figure Legend Snippet: Enhanced expression of long noncoding RNA HEIH (lncRNA-HEIH) promotes colorectal cancer tumorigenesis. (A) The expression of lncRNA-HEIH in lncRNA-HEIH stably overexpressed and control HT-29 cells was detected by quantitative real-time polymerase chain reaction and normalized to glyceraldehyde 3-phosphat e dehydrogenase. (B) Cell proliferation rate of lncRNA-HEIH stably overexpressed and control HT-29 cells were detected by the Cell Counting Kit-8 assays. (C) Proliferative cells of lncRNA-HEIH stably overexpressed and control HT-29 were labeled with ethynyl deoxyuridine (EdU). Red color indicts EdU-positive cells. Scale bars=100 μm. (D) The level of apoptosis in lncRNA-HEIH stably overexpressed and control HT-29 cells was detected by TdT-mediated dUTP nick end labeling (TUNEL) staining. Blue color indicts TUNEL-positive cells. Scale bars=100 μm. For A-D, results are shown as mean±standard deviation (SD). from three independent experiments. **p

    Techniques Used: Expressing, Stable Transfection, Real-time Polymerase Chain Reaction, Cell Counting, Labeling, End Labeling, TUNEL Assay, Staining, Standard Deviation

    18) Product Images from "Long non-coding RNA PART1 promotes intervertebral disc degeneration through regulating the miR-93/MMP2 pathway in nucleus pulposus cells"

    Article Title: Long non-coding RNA PART1 promotes intervertebral disc degeneration through regulating the miR-93/MMP2 pathway in nucleus pulposus cells

    Journal: International Journal of Molecular Medicine

    doi: 10.3892/ijmm.2020.4580

    LncRNA PART1 regulated cell growth, apoptosis and ECM-related genes through targeting miR-93-5p. (A) Images of NP cell colonies. The colony formation rates are shown on the right. (B) The apoptosis of NP cells was measured by flow cytometry. The apoptosis rates of NP cells are shown on the right. (C and D) The expression levels of Ki67 and C-caspase-3 in NP cells were measured by western blotting. (E-G) The expression levels of aggrecan, ADAMTS4, collagen II and MMP13 in NP cells were measured by (E and F) western blotting and (G) reverse transcription-quantitative PCR analysis. ** P
    Figure Legend Snippet: LncRNA PART1 regulated cell growth, apoptosis and ECM-related genes through targeting miR-93-5p. (A) Images of NP cell colonies. The colony formation rates are shown on the right. (B) The apoptosis of NP cells was measured by flow cytometry. The apoptosis rates of NP cells are shown on the right. (C and D) The expression levels of Ki67 and C-caspase-3 in NP cells were measured by western blotting. (E-G) The expression levels of aggrecan, ADAMTS4, collagen II and MMP13 in NP cells were measured by (E and F) western blotting and (G) reverse transcription-quantitative PCR analysis. ** P

    Techniques Used: Flow Cytometry, Expressing, Western Blot, Real-time Polymerase Chain Reaction

    19) Product Images from "Wild-type p53-induced phosphatase 1 promotes vascular smooth muscle cell proliferation and neointima hyperplasia after vascular injury via p-adenosine 5′-monophosphate-activated protein kinase/mammalian target of rapamycin complex 1 pathway"

    Article Title: Wild-type p53-induced phosphatase 1 promotes vascular smooth muscle cell proliferation and neointima hyperplasia after vascular injury via p-adenosine 5′-monophosphate-activated protein kinase/mammalian target of rapamycin complex 1 pathway

    Journal: Journal of Hypertension

    doi: 10.1097/HJH.0000000000002159

    Mammalian target of rapamycin complex 1 activity is positively regulated by wild-type p53-induced phosphatase 1 in vascular smooth muscle cells treated by PDGF-BB and carotid arteries after wire injury. (a) The protein expression of p-S6 Ser235/236 , S6, p-4EBP1 Thr37/46 , 4EBP1 and β-actin in common carotid arteries from C57BL/6J mice at day 28 after sham operation or wire injury with or without GSK treatment were analyzed by immunoblotting. Representative bands (upper panel) and corresponding quantification (lower panel) were shown ( n = 3). (b) Representative HE staining of carotid arteries from C57BL/6J mice at day 28 after sham operation or wire injury with physiological saline, GSK, Rapa (5 mg/kg) or GSK plus Rapa treatment (upper panel) and corresponding quantification for ratio of intima/media (lower panel) were shown ( n = 4). Magnification 200×. (c) The protein expression of p-S6 Ser235/236 , S6, p-4EBP1 Thr37/46 , 4EBP1 and β-actin were evaluated by immunoblotting in VSMCs incubated with physiological saline, GSK, PDGF-BB or PDGF-BB plus GSK for 48 h. Representative bands (upper panel) and corresponding quantification (lower panel) were shown ( n = 3). (d) VSMCs treated by physiological saline, GSK, Rapa or GSK plus Rapa for 48 h with or without PDGF-BB incubation were stained with SM α-actin (red), Ki-67 (green) and DAPI (blue). Representative images (upper panel) and corresponding quantification of Ki-67 positive VSMCs (lower panel) were shown ( n = 5). Magnification 400×. Data are shown as mean ± SD. ∗ P
    Figure Legend Snippet: Mammalian target of rapamycin complex 1 activity is positively regulated by wild-type p53-induced phosphatase 1 in vascular smooth muscle cells treated by PDGF-BB and carotid arteries after wire injury. (a) The protein expression of p-S6 Ser235/236 , S6, p-4EBP1 Thr37/46 , 4EBP1 and β-actin in common carotid arteries from C57BL/6J mice at day 28 after sham operation or wire injury with or without GSK treatment were analyzed by immunoblotting. Representative bands (upper panel) and corresponding quantification (lower panel) were shown ( n = 3). (b) Representative HE staining of carotid arteries from C57BL/6J mice at day 28 after sham operation or wire injury with physiological saline, GSK, Rapa (5 mg/kg) or GSK plus Rapa treatment (upper panel) and corresponding quantification for ratio of intima/media (lower panel) were shown ( n = 4). Magnification 200×. (c) The protein expression of p-S6 Ser235/236 , S6, p-4EBP1 Thr37/46 , 4EBP1 and β-actin were evaluated by immunoblotting in VSMCs incubated with physiological saline, GSK, PDGF-BB or PDGF-BB plus GSK for 48 h. Representative bands (upper panel) and corresponding quantification (lower panel) were shown ( n = 3). (d) VSMCs treated by physiological saline, GSK, Rapa or GSK plus Rapa for 48 h with or without PDGF-BB incubation were stained with SM α-actin (red), Ki-67 (green) and DAPI (blue). Representative images (upper panel) and corresponding quantification of Ki-67 positive VSMCs (lower panel) were shown ( n = 5). Magnification 400×. Data are shown as mean ± SD. ∗ P

    Techniques Used: Activity Assay, Expressing, Mouse Assay, Staining, Incubation

    Wild-type p53-induced phosphatase 1 inhibition suppresses vascular smooth muscle cell proliferation but not migration induced by PDGF-BB. (a) The relative mRNA level of Wip1 was detected by qRT-PCR in VSMCs after 48 h of physiological saline or PDGF-BB (30 ng/ml) treatment ( n = 4). (b) The protein expression of Wip1 and β-actin were determined by immunoblotting in VSMCs after 48 h of physiological saline or PDGF-BB treatment ( n = 4). (c) VSMC proliferation was analyzed via CCK-8 assay. VSMCs were incubated with physiological saline, GSK (50 μmol/l), PDGF-BB or PDGF-BB with GSK for 48 h. Then, the absorbance at 450 nm was obtained ( n = 5). (d) VSMCs treated as above described were stained with SM α-actin (red), Ki-67 (green) and DAPI (blue). Representative images (left) and corresponding quantification of Ki-67 positive VSMCs (right) were shown ( n = 5). Magnification 400×. (e) Migration of VSMCs treated with physiological saline, GSK, PDGF-BB or PDGF-BB plus GSK for 24 h was measured via wound healing assay. Representative images (upper panel) and corresponding quantification of healing rates (lower panel) were shown ( n = 4). Magnification 100×. (f) VSMCs were treated with physiological saline, GSK, PDGF-BB or PDGF-BB plus GSK for 8 h and migration was assessed by transwell assay. Representative images (upper panel) and corresponding quantification of migration cells (lower panel) were shown ( n = 4). Magnification 100×. Data are shown as mean ± SD. ∗ P
    Figure Legend Snippet: Wild-type p53-induced phosphatase 1 inhibition suppresses vascular smooth muscle cell proliferation but not migration induced by PDGF-BB. (a) The relative mRNA level of Wip1 was detected by qRT-PCR in VSMCs after 48 h of physiological saline or PDGF-BB (30 ng/ml) treatment ( n = 4). (b) The protein expression of Wip1 and β-actin were determined by immunoblotting in VSMCs after 48 h of physiological saline or PDGF-BB treatment ( n = 4). (c) VSMC proliferation was analyzed via CCK-8 assay. VSMCs were incubated with physiological saline, GSK (50 μmol/l), PDGF-BB or PDGF-BB with GSK for 48 h. Then, the absorbance at 450 nm was obtained ( n = 5). (d) VSMCs treated as above described were stained with SM α-actin (red), Ki-67 (green) and DAPI (blue). Representative images (left) and corresponding quantification of Ki-67 positive VSMCs (right) were shown ( n = 5). Magnification 400×. (e) Migration of VSMCs treated with physiological saline, GSK, PDGF-BB or PDGF-BB plus GSK for 24 h was measured via wound healing assay. Representative images (upper panel) and corresponding quantification of healing rates (lower panel) were shown ( n = 4). Magnification 100×. (f) VSMCs were treated with physiological saline, GSK, PDGF-BB or PDGF-BB plus GSK for 8 h and migration was assessed by transwell assay. Representative images (upper panel) and corresponding quantification of migration cells (lower panel) were shown ( n = 4). Magnification 100×. Data are shown as mean ± SD. ∗ P

    Techniques Used: Inhibition, Migration, Quantitative RT-PCR, Expressing, CCK-8 Assay, Incubation, Staining, Wound Healing Assay, Transwell Assay

    p-Adenosine 5′-monophosphate-activated protein kinase dephosphorylation blocked the inhibitory role of wild-type p53-induced phosphatase 1 ablation in vascular smooth muscle cell proliferation induced by PDGF-BB. (a) The protein expression of p-AMPKα Thr172 , AMPKα, p-AKT Thr308 , AKT and β-actin were evaluated by immunoblotting in VSMCs incubated with physiological saline, GSK, PDGF-BB or PDGF-BB plus GSK for 48 h. Representative bands (upper panel) and corresponding quantification (lower panel) were shown ( n = 3). (b) The protein expression of p-AMPKα Thr172 , AMPKα, p-S6 Ser235/236 , S6, p-4EBP1 Thr37/46 , 4EBP1 and β-actin were evaluated by immunoblotting in VSMCs treated by physiological saline, GSK, CC (15 μM) or GSK plus CC for 48 h with or without PDGF-BB. Representative bands (upper panel) and corresponding quantification (lower panel) were shown ( n = 3). (c) VSMCs treated by physiological saline, GSK, CC or GSK plus CC for 48 h with or without PDGF-BB incubation were stained with SM α-actin (red), Ki-67 (green) and DAPI (blue). Representative images (left) and corresponding quantification of Ki-67-positive VSMCs (right) were shown ( n = 5). Magnification 400×. Data are shown as mean ± S.D. ∗ P
    Figure Legend Snippet: p-Adenosine 5′-monophosphate-activated protein kinase dephosphorylation blocked the inhibitory role of wild-type p53-induced phosphatase 1 ablation in vascular smooth muscle cell proliferation induced by PDGF-BB. (a) The protein expression of p-AMPKα Thr172 , AMPKα, p-AKT Thr308 , AKT and β-actin were evaluated by immunoblotting in VSMCs incubated with physiological saline, GSK, PDGF-BB or PDGF-BB plus GSK for 48 h. Representative bands (upper panel) and corresponding quantification (lower panel) were shown ( n = 3). (b) The protein expression of p-AMPKα Thr172 , AMPKα, p-S6 Ser235/236 , S6, p-4EBP1 Thr37/46 , 4EBP1 and β-actin were evaluated by immunoblotting in VSMCs treated by physiological saline, GSK, CC (15 μM) or GSK plus CC for 48 h with or without PDGF-BB. Representative bands (upper panel) and corresponding quantification (lower panel) were shown ( n = 3). (c) VSMCs treated by physiological saline, GSK, CC or GSK plus CC for 48 h with or without PDGF-BB incubation were stained with SM α-actin (red), Ki-67 (green) and DAPI (blue). Representative images (left) and corresponding quantification of Ki-67-positive VSMCs (right) were shown ( n = 5). Magnification 400×. Data are shown as mean ± S.D. ∗ P

    Techniques Used: De-Phosphorylation Assay, Expressing, Incubation, Staining

    Tuberous sclerosis 1 knockdown abolished the repressive effects of wild-type p53-induced phosphatase 1 inhibition on vascular smooth muscle cell proliferation and neointima hyperplasia. (a) The protein expression of p-S6 Ser235/236 , S6, p-4EBP1 Thr37/46 , 4EBP1 and β-actin in common carotid arteries from Tsc1 WT or Tsc1 KD mice. Representative bands (left) and corresponding quantification (right) were shown ( n = 3). (b) Representative HE staining of carotid arteries from Tsc1 WT or Tsc1 KD mice at day 28 after sham operation or wire injury with or without GSK treatment (upper panel) and corresponding quantification for ratio of intima/media (lower panel) were shown ( n = 3). Magnification 200×. (c) The protein expression of p-S6 Ser235/236 , S6, p-4EBP1 Thr37/46 , 4EBP1 and β-actin in VSMCs isolated from Tsc1 WT or Tsc1 KD mice. Representative bands (left) and corresponding quantification (right) were shown ( n = 3). (d) VSMCs isolated from Tsc1 WT or Tsc1 KD mice were incubated with physiological saline, GSK, PDGF-BB or PDGF-BB plus GSK for 48 h and then stained with SM α-actin (red), Ki-67 (green) and DAPI (blue). Representative images (upper panel) and corresponding quantification of Ki-67-positive VSMCs (lower panel) were shown ( n = 5). Magnification 400×. Data are shown as mean ± SD. ∗ P
    Figure Legend Snippet: Tuberous sclerosis 1 knockdown abolished the repressive effects of wild-type p53-induced phosphatase 1 inhibition on vascular smooth muscle cell proliferation and neointima hyperplasia. (a) The protein expression of p-S6 Ser235/236 , S6, p-4EBP1 Thr37/46 , 4EBP1 and β-actin in common carotid arteries from Tsc1 WT or Tsc1 KD mice. Representative bands (left) and corresponding quantification (right) were shown ( n = 3). (b) Representative HE staining of carotid arteries from Tsc1 WT or Tsc1 KD mice at day 28 after sham operation or wire injury with or without GSK treatment (upper panel) and corresponding quantification for ratio of intima/media (lower panel) were shown ( n = 3). Magnification 200×. (c) The protein expression of p-S6 Ser235/236 , S6, p-4EBP1 Thr37/46 , 4EBP1 and β-actin in VSMCs isolated from Tsc1 WT or Tsc1 KD mice. Representative bands (left) and corresponding quantification (right) were shown ( n = 3). (d) VSMCs isolated from Tsc1 WT or Tsc1 KD mice were incubated with physiological saline, GSK, PDGF-BB or PDGF-BB plus GSK for 48 h and then stained with SM α-actin (red), Ki-67 (green) and DAPI (blue). Representative images (upper panel) and corresponding quantification of Ki-67-positive VSMCs (lower panel) were shown ( n = 5). Magnification 400×. Data are shown as mean ± SD. ∗ P

    Techniques Used: Inhibition, Expressing, Mouse Assay, Staining, Isolation, Incubation

    Wip1 inhibition ameliorates neointima hyperplasia and vascular restenosis after wire injury. (a) The relative mRNA level of Wip1 in common carotid arteries from C57BL/6J mice at day 28 after sham operation or wire injury was determined by qRT-PCR ( n = 4). (b) The protein expression of Wip1 and β-actin in common carotid arteries from C57BL/6J mice at day 28 after sham operation or wire injury were analyzed by immunoblotting ( n = 4). (c) Representative HE staining of carotid arteries from C57BL/6J mice at day 28 after sham operation or wire injury with or without GSK (25 mg/kg) treatment (left) and corresponding quantification for ratio of intima/media (right) ( n = 4). Magnification 200×. (d) Immunohistochemistry staining of Ki-67 (brown) in sections of carotid arteries from C57BL/6J mice at day 28 after sham operation or wire injury with or without GSK treatment (left) and corresponding quantification for Ki-67 positive cells within neointima (right) ( n = 4). Magnification 200×. (e) The relative mRNA levels of Collagen I and Collagen III in common carotid arteries from C57BL/6J mice at day 28 after sham operation or wire injury with or without GSK treatment were determined by qRT-PCR ( n = 4). Data are shown as mean ± SD. ∗ P
    Figure Legend Snippet: Wip1 inhibition ameliorates neointima hyperplasia and vascular restenosis after wire injury. (a) The relative mRNA level of Wip1 in common carotid arteries from C57BL/6J mice at day 28 after sham operation or wire injury was determined by qRT-PCR ( n = 4). (b) The protein expression of Wip1 and β-actin in common carotid arteries from C57BL/6J mice at day 28 after sham operation or wire injury were analyzed by immunoblotting ( n = 4). (c) Representative HE staining of carotid arteries from C57BL/6J mice at day 28 after sham operation or wire injury with or without GSK (25 mg/kg) treatment (left) and corresponding quantification for ratio of intima/media (right) ( n = 4). Magnification 200×. (d) Immunohistochemistry staining of Ki-67 (brown) in sections of carotid arteries from C57BL/6J mice at day 28 after sham operation or wire injury with or without GSK treatment (left) and corresponding quantification for Ki-67 positive cells within neointima (right) ( n = 4). Magnification 200×. (e) The relative mRNA levels of Collagen I and Collagen III in common carotid arteries from C57BL/6J mice at day 28 after sham operation or wire injury with or without GSK treatment were determined by qRT-PCR ( n = 4). Data are shown as mean ± SD. ∗ P

    Techniques Used: Inhibition, Mouse Assay, Quantitative RT-PCR, Expressing, Staining, Immunohistochemistry

    20) Product Images from "Annexin A1 promotes the progression of bladder cancer via regulating EGFR signaling pathway"

    Article Title: Annexin A1 promotes the progression of bladder cancer via regulating EGFR signaling pathway

    Journal: Cancer Cell International

    doi: 10.1186/s12935-021-02427-4

    Knockdown of ANXA1 inhibits tumor growth in subcutaneous xenograft models. A Gross appearance of tumors from NCG mice injected with 5637 NC or 5637 sh- ANXA1 cells. B Tumor growth was monitored for 30 days. The tumor volume of each group is shown as a line chart. C Individual value plot shows the tumor weights of the NC and sh- ANXA1 groups. D Representative IHC staining patterns of ANXA1, P-EGFR and Ki-67 in each group are shown (original magnification 200 ×) (scale bar: 50 μm). E Quantification of the number of Ki-67 positive cells in each group. F Proposed possible mechanism of ANXA1 functions in BLCA. ANXA1 promotes EGFR expression and inhibits P-EGFR degradation to activate EGFR signaling and its downstream pathways, thereby facilitating the proliferation, invasion and migration of BLCA cells
    Figure Legend Snippet: Knockdown of ANXA1 inhibits tumor growth in subcutaneous xenograft models. A Gross appearance of tumors from NCG mice injected with 5637 NC or 5637 sh- ANXA1 cells. B Tumor growth was monitored for 30 days. The tumor volume of each group is shown as a line chart. C Individual value plot shows the tumor weights of the NC and sh- ANXA1 groups. D Representative IHC staining patterns of ANXA1, P-EGFR and Ki-67 in each group are shown (original magnification 200 ×) (scale bar: 50 μm). E Quantification of the number of Ki-67 positive cells in each group. F Proposed possible mechanism of ANXA1 functions in BLCA. ANXA1 promotes EGFR expression and inhibits P-EGFR degradation to activate EGFR signaling and its downstream pathways, thereby facilitating the proliferation, invasion and migration of BLCA cells

    Techniques Used: Mouse Assay, Injection, Immunohistochemistry, Staining, Expressing, Migration

    21) Product Images from "Novel Aurora A Kinase Inhibitor Fangchinoline Enhances Cisplatin–DNA Adducts and Cisplatin Therapeutic Efficacy in OVCAR-3 Ovarian Cancer Cells-Derived Xenograft Model"

    Article Title: Novel Aurora A Kinase Inhibitor Fangchinoline Enhances Cisplatin–DNA Adducts and Cisplatin Therapeutic Efficacy in OVCAR-3 Ovarian Cancer Cells-Derived Xenograft Model

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms23031868

    Protein detection in tumor tissue. Tumors were collected on Day22. Aurora A activation was observed by detecting Aurora A and phospho (p)-Aurora A protein expressions in tumor tissue ( A ). Apoptosis and proliferation were evaluated by detecting cleaved caspase 3 and Ki67 protein expressions, respectively ( B ). Immunohistochemical staining was performed. Proteins were observed with brown staining. Original magnification, ×100. Scale bar: 200 μm.
    Figure Legend Snippet: Protein detection in tumor tissue. Tumors were collected on Day22. Aurora A activation was observed by detecting Aurora A and phospho (p)-Aurora A protein expressions in tumor tissue ( A ). Apoptosis and proliferation were evaluated by detecting cleaved caspase 3 and Ki67 protein expressions, respectively ( B ). Immunohistochemical staining was performed. Proteins were observed with brown staining. Original magnification, ×100. Scale bar: 200 μm.

    Techniques Used: Activation Assay, Immunohistochemistry, Staining

    22) Product Images from "Systematic analysis uncovers SYK dependency in NF1LoF melanoma cells"

    Article Title: Systematic analysis uncovers SYK dependency in NF1LoF melanoma cells

    Journal: bioRxiv

    doi: 10.1101/2022.03.06.483170

    MTX-216 co-suppresses Ki-67 and p-S6 and induces apoptosis in NF1 LoF cells. (a, b) MTX-216 dose-dependent changes in apoptotic response of COLO792 cells (after 48 h) and WM3918 and MeWo cells (after 72 h), measured using a NucView Caspase-3 reporter assay. Single-cell NucView intensities across different inhibitor doses (a) and the estimation of the percentage of apoptotic cells based on NucView intensity gating (b) are shown for each cell line. Data are presented as mean values ± s.d. calculated across n = 2 replicates. (c) Two-sided Pearson’s correlation analysis between the percentage of p-S6 Low/ Ki-67 Low cells and the inhibitor-induced normalized growth rate (measured after 72 h of treatment) across three NF1 LoF /BRAF WT melanoma cell lines (MeWo, WM3918 and COLO792) and one NF1 WT /BRAF V600E cell line (COLO858) treated with MTX-216, trametinib, ulixertinib and pictilisib (at the same concentrations as shown in Fig. 1b ). (d) Co-variate single-cell analysis of p-S6 versus Ki-67 across three NF1 LoF /BRAF WT melanoma cell lines (MeWo, WM3918 and COLO792) and one NF1 WT /BRAF V600E cell line (COLO858) treated for 72 h with indicated concentrations of MTX-216, trametinib, ulixertinib and pictilisib. The horizontal and vertical dash lines were used to gate Ki-67 High versus Ki-67 Low cells and p-S6 High versus p-S6 Low cells, respectively. Percentages of cells in each quadrant are shown in red.
    Figure Legend Snippet: MTX-216 co-suppresses Ki-67 and p-S6 and induces apoptosis in NF1 LoF cells. (a, b) MTX-216 dose-dependent changes in apoptotic response of COLO792 cells (after 48 h) and WM3918 and MeWo cells (after 72 h), measured using a NucView Caspase-3 reporter assay. Single-cell NucView intensities across different inhibitor doses (a) and the estimation of the percentage of apoptotic cells based on NucView intensity gating (b) are shown for each cell line. Data are presented as mean values ± s.d. calculated across n = 2 replicates. (c) Two-sided Pearson’s correlation analysis between the percentage of p-S6 Low/ Ki-67 Low cells and the inhibitor-induced normalized growth rate (measured after 72 h of treatment) across three NF1 LoF /BRAF WT melanoma cell lines (MeWo, WM3918 and COLO792) and one NF1 WT /BRAF V600E cell line (COLO858) treated with MTX-216, trametinib, ulixertinib and pictilisib (at the same concentrations as shown in Fig. 1b ). (d) Co-variate single-cell analysis of p-S6 versus Ki-67 across three NF1 LoF /BRAF WT melanoma cell lines (MeWo, WM3918 and COLO792) and one NF1 WT /BRAF V600E cell line (COLO858) treated for 72 h with indicated concentrations of MTX-216, trametinib, ulixertinib and pictilisib. The horizontal and vertical dash lines were used to gate Ki-67 High versus Ki-67 Low cells and p-S6 High versus p-S6 Low cells, respectively. Percentages of cells in each quadrant are shown in red.

    Techniques Used: Reporter Assay, Single-cell Analysis

    23) Product Images from "WNT11-FZD7-DAAM1 signalling supports tumour initiating abilities and melanoma amoeboid invasion"

    Article Title: WNT11-FZD7-DAAM1 signalling supports tumour initiating abilities and melanoma amoeboid invasion

    Journal: Nature Communications

    doi: 10.1038/s41467-020-18951-2

    FZD7-DAAM1-RhoA-ROCK1/2 supports tumour initiation and metastasis in vivo. a Schematic of experiment (left) and tumour weight (right) of ROCKi (H1152 or GSK269962A) pre-treated A375M2 cells 18 days post-subcutaneous injection into NSG mice ( n = 5 mice for control and H1152, n = 4 for GSK269962A). b – d Quantification of b melanoma cell shape score, c H-score of p-MLC2 staining and d ki-67 positive cells in A375M2 tumours from ( a ). e Limiting dilution assay estimating TIF (top) and tumour volume (bottom) of shControl and sh FZD7 WM1361 cells when injected at different dilutions (500,000, 50,000 and 5,000 cells) into NSG mice (Number of tumours per condition indicated in table). TIF was determined using ELDA. f – h Representative images (top) and quantification (bottom) of f melanoma cell shape score, g H-score of p-MLC2 staining and h ki-67 positive cells in TB and IF of shControl ( n = 16) and sh FZD7 ( n = 9) derived tumours from 50,000 cells’ condition from ( e ). Scale bar, 100 μm; inset, 25 μm. i Limiting dilution assay estimating TIF (top) and tumour volume (bottom) of shControl and sh DAAM1 WM1361 cells when injected at different dilutions (500,000, 50,000 and 5,000 cells) into NSG mice (Number of tumours per condition indicated in table). TIF was determined using ELDA. j – l Representative images (top) and quantification (bottom) of j melanoma cell shape score, k H-score of p-MLC2 staining and l ki-67 positive cells in TB and IF of shControl ( n = 10) and sh DAAM1 ( n = 5) derived tumours from 50,000 cells’ condition from ( i ). Scale bar, 100 μm; inset, 25 μm. m Representative confocal images (left) and percentage of fluorescence area (right) of mouse lungs 24 h ( n = 6 mice) and 3 weeks ( n = 5 mice) after tail vein injection into NSG mice of WM1361 cells expressing shControl and sh DAAM1 . Scale bar, 50 μm. a , m Graphs show mean ± s.e.m. b – l Box limits show 25th and 75th percentiles, the horizontal line shows the median, and whiskers show minimum and maximum range of values. a – d One-way ANOVA with Dunnett post-hoc test. e , i Two-tailed Mann–Whitney test. f – h , j – l One-way ANOVA with Tukey post-hoc test. m Two-tailed t -test. For all graphs, * p
    Figure Legend Snippet: FZD7-DAAM1-RhoA-ROCK1/2 supports tumour initiation and metastasis in vivo. a Schematic of experiment (left) and tumour weight (right) of ROCKi (H1152 or GSK269962A) pre-treated A375M2 cells 18 days post-subcutaneous injection into NSG mice ( n = 5 mice for control and H1152, n = 4 for GSK269962A). b – d Quantification of b melanoma cell shape score, c H-score of p-MLC2 staining and d ki-67 positive cells in A375M2 tumours from ( a ). e Limiting dilution assay estimating TIF (top) and tumour volume (bottom) of shControl and sh FZD7 WM1361 cells when injected at different dilutions (500,000, 50,000 and 5,000 cells) into NSG mice (Number of tumours per condition indicated in table). TIF was determined using ELDA. f – h Representative images (top) and quantification (bottom) of f melanoma cell shape score, g H-score of p-MLC2 staining and h ki-67 positive cells in TB and IF of shControl ( n = 16) and sh FZD7 ( n = 9) derived tumours from 50,000 cells’ condition from ( e ). Scale bar, 100 μm; inset, 25 μm. i Limiting dilution assay estimating TIF (top) and tumour volume (bottom) of shControl and sh DAAM1 WM1361 cells when injected at different dilutions (500,000, 50,000 and 5,000 cells) into NSG mice (Number of tumours per condition indicated in table). TIF was determined using ELDA. j – l Representative images (top) and quantification (bottom) of j melanoma cell shape score, k H-score of p-MLC2 staining and l ki-67 positive cells in TB and IF of shControl ( n = 10) and sh DAAM1 ( n = 5) derived tumours from 50,000 cells’ condition from ( i ). Scale bar, 100 μm; inset, 25 μm. m Representative confocal images (left) and percentage of fluorescence area (right) of mouse lungs 24 h ( n = 6 mice) and 3 weeks ( n = 5 mice) after tail vein injection into NSG mice of WM1361 cells expressing shControl and sh DAAM1 . Scale bar, 50 μm. a , m Graphs show mean ± s.e.m. b – l Box limits show 25th and 75th percentiles, the horizontal line shows the median, and whiskers show minimum and maximum range of values. a – d One-way ANOVA with Dunnett post-hoc test. e , i Two-tailed Mann–Whitney test. f – h , j – l One-way ANOVA with Tukey post-hoc test. m Two-tailed t -test. For all graphs, * p

    Techniques Used: In Vivo, Injection, Mouse Assay, Staining, Limiting Dilution Assay, Derivative Assay, Fluorescence, Expressing, Two Tailed Test, MANN-WHITNEY

    Analysis of the invasive front of human metastatic melanomas. a – i Representative images (left) and quantification (right) of a melanoma cell shape score, b H-score of p-MLC2 staining, c ki-67 positive cells, H-score of d DAAM1, e WNT11, f WNT5B, g ALDH1A1, h CD44 and i NANOG staining in matched TB and IF from melanoma metastases. j Model summarizing the findings of this study. The IF of human primary melanomas is enriched in cells with rounded-amoeboid morphology, high levels of Myosin II, proliferative, non-canonical Wnt and cancer stem cell-related markers. This phenotype is recapitulated and further enriched in melanoma metastasis. WNT11/5B activate FZD7 and DAAM1 to control Rho activity and then ROCK1/2-Myosin II levels. All these signalling components have an impact on amoeboid features and tumour initiation in melanoma both in vitro and in vivo. Specifically, DAAM1 plays an essential role in tumour and metastasis initiation and subsequent metastatic outgrowth by sustaining the amoeboid phenotype. a – i 45 metastatic melanomas. a , e – i Scale bar, 100 μm; inset, 50 μm. b – d Scale bar, 300 μm. a – i Box limits show 25th and 75th percentiles, the horizontal line shows the median, and whiskers show minimum and maximum range of values. a , b , d – f Two-tailed paired t -test. c , g – i Two-tailed Wilcoxon test. Human schematic in this figure was created using Servier Medical Art templates licensed under a Creative Commons Attribution 3.0 Unported License ( https://smart.servier.com ).
    Figure Legend Snippet: Analysis of the invasive front of human metastatic melanomas. a – i Representative images (left) and quantification (right) of a melanoma cell shape score, b H-score of p-MLC2 staining, c ki-67 positive cells, H-score of d DAAM1, e WNT11, f WNT5B, g ALDH1A1, h CD44 and i NANOG staining in matched TB and IF from melanoma metastases. j Model summarizing the findings of this study. The IF of human primary melanomas is enriched in cells with rounded-amoeboid morphology, high levels of Myosin II, proliferative, non-canonical Wnt and cancer stem cell-related markers. This phenotype is recapitulated and further enriched in melanoma metastasis. WNT11/5B activate FZD7 and DAAM1 to control Rho activity and then ROCK1/2-Myosin II levels. All these signalling components have an impact on amoeboid features and tumour initiation in melanoma both in vitro and in vivo. Specifically, DAAM1 plays an essential role in tumour and metastasis initiation and subsequent metastatic outgrowth by sustaining the amoeboid phenotype. a – i 45 metastatic melanomas. a , e – i Scale bar, 100 μm; inset, 50 μm. b – d Scale bar, 300 μm. a – i Box limits show 25th and 75th percentiles, the horizontal line shows the median, and whiskers show minimum and maximum range of values. a , b , d – f Two-tailed paired t -test. c , g – i Two-tailed Wilcoxon test. Human schematic in this figure was created using Servier Medical Art templates licensed under a Creative Commons Attribution 3.0 Unported License ( https://smart.servier.com ).

    Techniques Used: Staining, Activity Assay, In Vitro, In Vivo, Two Tailed Test

    Amoeboid behaviour enhances tumour formation, tumour progression and metastasis in vivo. a Schematic of in vivo experiment with 4599 cells injected intradermally into NSG mice treated with ROCKi (25 mg/kg GSK269962A) or control (5% DMSO) ( n = 5 mice for control and n = 4 for ROCKi). b Representative H E images showing areas of TB, IF and local area of invasion into the dermis (distal invasive front (DIF)) of primary tumours derived from ( a ). Dashed lines represent the boundary between tumour areas. Scale bar, 200 μm. c Representative images (left) and quantification (right) of invading cells with co-staining of p-MLC2 (red) and ki-67 (green) at the DIF of control tumours from ( a ). Scale bar, 200 μm. Yellow arrows indicate ki-67 positive invading cells with p-MLC2 score 3 intensity. d – f Representative images (top) and quantification (bottom) of d melanoma cell shape score, e H-score and percentage of cells with score intensity 0–3 for p-MLC2 staining and f ki-67 positive cells in primary tumours from ( a ). Scale bar, 100 μm; inset, 25 μm. g GSEA plots showing enrichment of proliferative and invasive gene signatures from Verfaillie study 19 in A375M2 cells compared to A375M2 cells treated with ROCKi (H1152 and Y27632) and blebbistatin or to A375P cells 10 . NES, normalized enrichment score; FDR, false discovery rate. h Tumour growth curves of 4599 cells from ( a ). i Representative images (left) and QuPath mark-up (right) of mCherry staining and j quantification of invading cells into the dermis in primary tumours derived from ( a ). Dashed lines represent the boundary between IF and DIF. Scale bar, 50 μm. k Representative images (left) and quantification of tumour area (right) of spontaneous lung metastasis from ( a ). Scale bar, 1 mm. l , m Representative images of mouse lungs (left) and quantification of tumour area (right) at the indicated times after tail vein injection of 4599 cells l pre-treated with ROCKi for 24 h or m without any pre-treatment into NSG mice. Animals were systemically treated with ROCKi ( n = 6 mice/group). Scale bar, 2 mm; inset, 500 μm. c Graphs show mean ± s.e.m. d – f , j – m Box limits show 25th and 75th percentiles, the horizontal line shows the median, and whiskers show minimum and maximum range of values. d – f One-way ANOVA with Benjamini, Krieger and Yekutieli correction. h , j Two-tailed t -test. k – m Two-tailed Mann–Whitney test. For all graphs, * p
    Figure Legend Snippet: Amoeboid behaviour enhances tumour formation, tumour progression and metastasis in vivo. a Schematic of in vivo experiment with 4599 cells injected intradermally into NSG mice treated with ROCKi (25 mg/kg GSK269962A) or control (5% DMSO) ( n = 5 mice for control and n = 4 for ROCKi). b Representative H E images showing areas of TB, IF and local area of invasion into the dermis (distal invasive front (DIF)) of primary tumours derived from ( a ). Dashed lines represent the boundary between tumour areas. Scale bar, 200 μm. c Representative images (left) and quantification (right) of invading cells with co-staining of p-MLC2 (red) and ki-67 (green) at the DIF of control tumours from ( a ). Scale bar, 200 μm. Yellow arrows indicate ki-67 positive invading cells with p-MLC2 score 3 intensity. d – f Representative images (top) and quantification (bottom) of d melanoma cell shape score, e H-score and percentage of cells with score intensity 0–3 for p-MLC2 staining and f ki-67 positive cells in primary tumours from ( a ). Scale bar, 100 μm; inset, 25 μm. g GSEA plots showing enrichment of proliferative and invasive gene signatures from Verfaillie study 19 in A375M2 cells compared to A375M2 cells treated with ROCKi (H1152 and Y27632) and blebbistatin or to A375P cells 10 . NES, normalized enrichment score; FDR, false discovery rate. h Tumour growth curves of 4599 cells from ( a ). i Representative images (left) and QuPath mark-up (right) of mCherry staining and j quantification of invading cells into the dermis in primary tumours derived from ( a ). Dashed lines represent the boundary between IF and DIF. Scale bar, 50 μm. k Representative images (left) and quantification of tumour area (right) of spontaneous lung metastasis from ( a ). Scale bar, 1 mm. l , m Representative images of mouse lungs (left) and quantification of tumour area (right) at the indicated times after tail vein injection of 4599 cells l pre-treated with ROCKi for 24 h or m without any pre-treatment into NSG mice. Animals were systemically treated with ROCKi ( n = 6 mice/group). Scale bar, 2 mm; inset, 500 μm. c Graphs show mean ± s.e.m. d – f , j – m Box limits show 25th and 75th percentiles, the horizontal line shows the median, and whiskers show minimum and maximum range of values. d – f One-way ANOVA with Benjamini, Krieger and Yekutieli correction. h , j Two-tailed t -test. k – m Two-tailed Mann–Whitney test. For all graphs, * p

    Techniques Used: In Vivo, Injection, Mouse Assay, Derivative Assay, Staining, Two Tailed Test, MANN-WHITNEY

    Analysis of the invasive front of human primary melanomas. a – i Representative images (left) and quantification (right) of a melanoma cell shape score, b H-score of p-MLC2 staining, c ki-67 positive cells, H-score of d DAAM1, e WNT11, f WNT5B, g ALDH1A1, h CD44 and i NANOG staining in matched TB and IF from primary melanomas. j Principal component analysis (PCA) based on the expression of amoeboid (cell shape and p-MLC2), proliferative (ki-67), non-canonical Wnt pathway (WNT11, WNT5B and DAAM1) and cancer stem cell-related (ALDH1A1, CD44 and NANOG) markers assessed by immunohistochemistry in matched TB and IF from primary melanomas. Percentage of variation explained by each component is given in the axis labels. k , l Kaplan–Meier survival curves of k overall survival and l disease-free survival according to ALDH1A1 protein expression in the IF from our cohort of primary melanomas. ALDH1A1 expression was categorized as low or high using the median expression. a – l 53 primary melanomas. a , e – i Scale bar, 100 μm; inset, 50 μm. b – d Scale bar, 300 μm. a – i Box limits show 25th and 75th percentiles, the horizontal line shows the median, and whiskers show the minimum and maximum range of values. a , b , d – f Two-tailed paired t -test. c , g – i Two-tailed Wilcoxon test. j Scatter plot showing principal components 1 (PC1) and 2 (PC2). k , l Log-rank test. Human schematic in this figure was created using Servier Medical Art templates licensed under a Creative Commons Attribution 3.0 Unported License ( https://smart.servier.com ).
    Figure Legend Snippet: Analysis of the invasive front of human primary melanomas. a – i Representative images (left) and quantification (right) of a melanoma cell shape score, b H-score of p-MLC2 staining, c ki-67 positive cells, H-score of d DAAM1, e WNT11, f WNT5B, g ALDH1A1, h CD44 and i NANOG staining in matched TB and IF from primary melanomas. j Principal component analysis (PCA) based on the expression of amoeboid (cell shape and p-MLC2), proliferative (ki-67), non-canonical Wnt pathway (WNT11, WNT5B and DAAM1) and cancer stem cell-related (ALDH1A1, CD44 and NANOG) markers assessed by immunohistochemistry in matched TB and IF from primary melanomas. Percentage of variation explained by each component is given in the axis labels. k , l Kaplan–Meier survival curves of k overall survival and l disease-free survival according to ALDH1A1 protein expression in the IF from our cohort of primary melanomas. ALDH1A1 expression was categorized as low or high using the median expression. a – l 53 primary melanomas. a , e – i Scale bar, 100 μm; inset, 50 μm. b – d Scale bar, 300 μm. a – i Box limits show 25th and 75th percentiles, the horizontal line shows the median, and whiskers show the minimum and maximum range of values. a , b , d – f Two-tailed paired t -test. c , g – i Two-tailed Wilcoxon test. j Scatter plot showing principal components 1 (PC1) and 2 (PC2). k , l Log-rank test. Human schematic in this figure was created using Servier Medical Art templates licensed under a Creative Commons Attribution 3.0 Unported License ( https://smart.servier.com ).

    Techniques Used: Staining, Expressing, Immunohistochemistry, Two Tailed Test

    Amoeboid cells support tumour initiation in melanoma in vitro and in vivo. a Heatmap displaying enrichment scores for differentially expressed stem cell-related signatures in amoeboid A375M2 cells compared to A375P cells or to A375M2 cells treated with ROCK1/2 inhibitors (ROCKi) (H1152 and Y27632) or blebbistatin using single-sample Gene Set Enrichment Analysis (ssGSEA). b , c Limiting dilution assay estimating b tumour-initiating frequency (TIF) and c tumour volume of A375M2 and A375P cells when injected at different dilutions (500,000, 50,000 and 5,000 cells) into NOD/SCID/IL2Rγ−/− (NSG) mice (Number of tumours per condition indicated in table). TIF was determined using ELDA. d , e Representative images (left) and quantification (right) of d melanoma cell shape score and e H-score of p-MLC2 staining in tumour body (TB) and invasive front (IF) of A375M2 ( n = 9) and A375P ( n = 8) tumours from 50,000 cells’ condition from ( b ). Scale bar, 100 μm; inset, 25 μm. f Representative phase-contrast images (top) and quantification of sphere formation index (bottom) of A375P ( n = 3) and WM983A cells ( n = 4) serially passaged. Scale bar, 250 μm. g , h Representative images (top) and quantification (bottom) of g H-score of p-MLC2 staining and h ki-67 positive cells in A375P and WM983A spheres serially passaged ( n = 4). Scale bar, 50 μm. i – k Representative i phase-contrast and j , k confocal images (top) and quantification (bottom) of i cell morphology ( > 250 cells pooled from n = 3), j p-MLC2 immunofluorescence signal normalized by cell area ( > 80 cells pooled from n = 4) and k percentage of blebbing cells (5 fields of view per experiment, > 75 cells per experiment, n = 3) of individual A375P and WM983A cells from adherent conditions (P0) and from dissociated cells from spheres serially passaged (P1–P3) on collagen I matrix. Scale bar, i , j 50 μm and k 20 μm. c – e , i , j Box limits show 25th and 75th percentiles, the horizontal line shows the median, and whiskers show the minimum and maximum range of values. f – h , k Graphs show mean ± s.e.m. f – k n means number of independent biological experiments. c two-tailed t -test. d – h , k One-way ANOVA with Tukey post-hoc test. i , j Kruskal–Wallis with Dunn’s multiple comparison test. For all graphs, * p
    Figure Legend Snippet: Amoeboid cells support tumour initiation in melanoma in vitro and in vivo. a Heatmap displaying enrichment scores for differentially expressed stem cell-related signatures in amoeboid A375M2 cells compared to A375P cells or to A375M2 cells treated with ROCK1/2 inhibitors (ROCKi) (H1152 and Y27632) or blebbistatin using single-sample Gene Set Enrichment Analysis (ssGSEA). b , c Limiting dilution assay estimating b tumour-initiating frequency (TIF) and c tumour volume of A375M2 and A375P cells when injected at different dilutions (500,000, 50,000 and 5,000 cells) into NOD/SCID/IL2Rγ−/− (NSG) mice (Number of tumours per condition indicated in table). TIF was determined using ELDA. d , e Representative images (left) and quantification (right) of d melanoma cell shape score and e H-score of p-MLC2 staining in tumour body (TB) and invasive front (IF) of A375M2 ( n = 9) and A375P ( n = 8) tumours from 50,000 cells’ condition from ( b ). Scale bar, 100 μm; inset, 25 μm. f Representative phase-contrast images (top) and quantification of sphere formation index (bottom) of A375P ( n = 3) and WM983A cells ( n = 4) serially passaged. Scale bar, 250 μm. g , h Representative images (top) and quantification (bottom) of g H-score of p-MLC2 staining and h ki-67 positive cells in A375P and WM983A spheres serially passaged ( n = 4). Scale bar, 50 μm. i – k Representative i phase-contrast and j , k confocal images (top) and quantification (bottom) of i cell morphology ( > 250 cells pooled from n = 3), j p-MLC2 immunofluorescence signal normalized by cell area ( > 80 cells pooled from n = 4) and k percentage of blebbing cells (5 fields of view per experiment, > 75 cells per experiment, n = 3) of individual A375P and WM983A cells from adherent conditions (P0) and from dissociated cells from spheres serially passaged (P1–P3) on collagen I matrix. Scale bar, i , j 50 μm and k 20 μm. c – e , i , j Box limits show 25th and 75th percentiles, the horizontal line shows the median, and whiskers show the minimum and maximum range of values. f – h , k Graphs show mean ± s.e.m. f – k n means number of independent biological experiments. c two-tailed t -test. d – h , k One-way ANOVA with Tukey post-hoc test. i , j Kruskal–Wallis with Dunn’s multiple comparison test. For all graphs, * p

    Techniques Used: In Vitro, In Vivo, Limiting Dilution Assay, Injection, Mouse Assay, Staining, Immunofluorescence, Two Tailed Test

    24) Product Images from "c-myc regulates the sensitivity of breast cancer cells to palbociclib via c-myc/miR-29b-3p/CDK6 axis"

    Article Title: c-myc regulates the sensitivity of breast cancer cells to palbociclib via c-myc/miR-29b-3p/CDK6 axis

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-020-02980-2

    Inhibition of c-myc sensitizes breast cancer cells to palbociclib in vivo. Empty vector or shMyc were transfected into MDA-MB-231 cells, which were injected into nude mice, respectively. Mice bearing MDA-MB-231 xenografts with a tumor volume of 100 mm 3 (6 for each group) was then randomly grouped and treated with vehicle (orally), or palbociclib at a dose of 100 mg/kg twice a week by oral gavage. a Visualization of the mice and tumors, after 21 days of initial treatment. b Tumor volumes were calculated every 3 days. c The qRT-PCR was performed to detect the average expression miR-29b-3p in xenograft tumors. d Western blot analysis of c-myc and CDK6 in xenograft tumors. GAPDH was used as an internal control. e The tumors were removed from the mice in 21 days after drug treatment ended, and immunohistochemical staining for CDK6, c-myc, and Ki-67 were conducted. Expression ratio of CDK6, c-myc, and ki67 in each of the treatment arms are shown. f Immunohistochemical staining of c-myc and Ki-67 in patient-derived tumor xenograft (PDX) model of patient 2 and 5. g The positive stained cells of Ki-67 before and after palbociclib treatment in all eight PDX models. Error bars indicate mean ± SD.
    Figure Legend Snippet: Inhibition of c-myc sensitizes breast cancer cells to palbociclib in vivo. Empty vector or shMyc were transfected into MDA-MB-231 cells, which were injected into nude mice, respectively. Mice bearing MDA-MB-231 xenografts with a tumor volume of 100 mm 3 (6 for each group) was then randomly grouped and treated with vehicle (orally), or palbociclib at a dose of 100 mg/kg twice a week by oral gavage. a Visualization of the mice and tumors, after 21 days of initial treatment. b Tumor volumes were calculated every 3 days. c The qRT-PCR was performed to detect the average expression miR-29b-3p in xenograft tumors. d Western blot analysis of c-myc and CDK6 in xenograft tumors. GAPDH was used as an internal control. e The tumors were removed from the mice in 21 days after drug treatment ended, and immunohistochemical staining for CDK6, c-myc, and Ki-67 were conducted. Expression ratio of CDK6, c-myc, and ki67 in each of the treatment arms are shown. f Immunohistochemical staining of c-myc and Ki-67 in patient-derived tumor xenograft (PDX) model of patient 2 and 5. g The positive stained cells of Ki-67 before and after palbociclib treatment in all eight PDX models. Error bars indicate mean ± SD.

    Techniques Used: Inhibition, In Vivo, Plasmid Preparation, Transfection, Multiple Displacement Amplification, Injection, Mouse Assay, Quantitative RT-PCR, Expressing, Western Blot, Immunohistochemistry, Staining, Derivative Assay

    25) Product Images from "Moxidectin inhibits glioma cell viability by inducing G0/G1 cell cycle arrest and apoptosis"

    Article Title: Moxidectin inhibits glioma cell viability by inducing G0/G1 cell cycle arrest and apoptosis

    Journal: Oncology Reports

    doi: 10.3892/or.2018.6561

    MOX suppressed U251 Xenograft growth in vivo . Nude mice with U251 subcutaneous tumor xenografts were treated with saline or 20 mg/kg MOX every day by peritoneal injection for 3 weeks. (A) The tumors were isolated and (B) volumes were measured. (C) Charting of mouse weight with time. (D) Hematoxylin and eosin staining, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay and representative immunohistochemistry images of Ki-67, cleaved caspase-3 and caspase-9 in U251 Xenograft tissues from vehicle or MOX-treated mice. (E) Quantitative analysis of Ki-67, cleaved caspase-3 and caspase-9-positive cells in xenograft tissues of different groups. (F) Relative amount of indicated proteins are presented. Data are presented as the mean ± SD. **P
    Figure Legend Snippet: MOX suppressed U251 Xenograft growth in vivo . Nude mice with U251 subcutaneous tumor xenografts were treated with saline or 20 mg/kg MOX every day by peritoneal injection for 3 weeks. (A) The tumors were isolated and (B) volumes were measured. (C) Charting of mouse weight with time. (D) Hematoxylin and eosin staining, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay and representative immunohistochemistry images of Ki-67, cleaved caspase-3 and caspase-9 in U251 Xenograft tissues from vehicle or MOX-treated mice. (E) Quantitative analysis of Ki-67, cleaved caspase-3 and caspase-9-positive cells in xenograft tissues of different groups. (F) Relative amount of indicated proteins are presented. Data are presented as the mean ± SD. **P

    Techniques Used: In Vivo, Mouse Assay, Injection, Isolation, Staining, End Labeling, Immunohistochemistry

    26) Product Images from "Metformin exhibits antiproliferation activity in breast cancer via miR-483-3p/METTL3/m6A/p21 pathway"

    Article Title: Metformin exhibits antiproliferation activity in breast cancer via miR-483-3p/METTL3/m6A/p21 pathway

    Journal: Oncogenesis

    doi: 10.1038/s41389-020-00290-y

    METTL3 promoted breast cancer cell proliferation by mediating p21 expression. A , B Silencing of p21 inhibited the increasing of p21 induced by METTL3 knockdown in both RNA and protein level in SUM-1315 and MCF-7 cells. The relative RNA level was calculated by the 2 − ΔΔCt method and normalized based on β-actin. The average mRNA level of p21 in the shNC group was set as 1. C – F Suppression of p21 alleviated the inhibitory effects on cell proliferation and colony formation mediated by METTL3. G IHC of subcutaneous xenograft tumors showed that a significant increase in the positive rate of Ki-67 while a significant decrease in the positive rate of p21 in the METTL3 overexpression group. H The protein level of METTL3 in the tumors of mice treated with metformin decreased than those with PBS, while the protein level of p21 increased in the metformin group. shNC, scramble control; shM3/shMETTL3-2, METTL3 knockdown; shM3 + siP21, METTL3 knockdown cells transfected with p21 siRNA; oeNC, negative control; oeNC-Met, oeNC-Met negative control group treated with metformin; oeMETTL3, METTL3 overexpression; oeMETTL3-Met, METTL3 overexpression group treated with metformin. Data represented the mean ± SD, * p
    Figure Legend Snippet: METTL3 promoted breast cancer cell proliferation by mediating p21 expression. A , B Silencing of p21 inhibited the increasing of p21 induced by METTL3 knockdown in both RNA and protein level in SUM-1315 and MCF-7 cells. The relative RNA level was calculated by the 2 − ΔΔCt method and normalized based on β-actin. The average mRNA level of p21 in the shNC group was set as 1. C – F Suppression of p21 alleviated the inhibitory effects on cell proliferation and colony formation mediated by METTL3. G IHC of subcutaneous xenograft tumors showed that a significant increase in the positive rate of Ki-67 while a significant decrease in the positive rate of p21 in the METTL3 overexpression group. H The protein level of METTL3 in the tumors of mice treated with metformin decreased than those with PBS, while the protein level of p21 increased in the metformin group. shNC, scramble control; shM3/shMETTL3-2, METTL3 knockdown; shM3 + siP21, METTL3 knockdown cells transfected with p21 siRNA; oeNC, negative control; oeNC-Met, oeNC-Met negative control group treated with metformin; oeMETTL3, METTL3 overexpression; oeMETTL3-Met, METTL3 overexpression group treated with metformin. Data represented the mean ± SD, * p

    Techniques Used: Expressing, Immunohistochemistry, Over Expression, Mouse Assay, Transfection, Negative Control

    27) Product Images from "Assessment of Histopathological Grade and Ki-67 Expression in Tobacco and Non-tobacco Habitual Buccal Mucosa Cancer"

    Article Title: Assessment of Histopathological Grade and Ki-67 Expression in Tobacco and Non-tobacco Habitual Buccal Mucosa Cancer

    Journal: Indian Journal of Otolaryngology and Head & Neck Surgery

    doi: 10.1007/s12070-018-1328-1

    The Ki-67 LI relation with tobacco and non-tobacco habits of buccal mucosa cancer. Independent t-test shows the highly significant association of Ki-67 LI in tobacco and non-tobacco habitual ( p = 0.000, p
    Figure Legend Snippet: The Ki-67 LI relation with tobacco and non-tobacco habits of buccal mucosa cancer. Independent t-test shows the highly significant association of Ki-67 LI in tobacco and non-tobacco habitual ( p = 0.000, p

    Techniques Used:

    28) Product Images from "Berberine Improves Chemo-Sensitivity to Cisplatin by Enhancing Cell Apoptosis and Repressing PI3K/AKT/mTOR Signaling Pathway in Gastric Cancer"

    Article Title: Berberine Improves Chemo-Sensitivity to Cisplatin by Enhancing Cell Apoptosis and Repressing PI3K/AKT/mTOR Signaling Pathway in Gastric Cancer

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2020.616251

    Berberine sensitizes DDP-resistance gastric cancer cells to cisplatin treatment in vivo . (A) In vivo tumor growth of SGC-7901/DDP cells in the nude mice after treatment with DDP (3 mg/kg, i.p.), berberine (10 mg/kg, i.p.) or DDP (3 mg/kg, i.p.) + Berberine (10 mg/kg, i.p.). (B) Tumor weight dissected from the nude mice after treatment with DDP (3 mg/kg, i.p.), berberine (10 mg/kg, i.p.) or DDP (3 mg/kg, i.p.) + Berberine (10 mg/kg, i.p.). (C) Immunostaining of Ki-67 in the tumor tissues from the mice after treatment with DDP (3 mg/kg, i.p.), berberine (10 mg/kg, i.p.) or DDP (3 mg/kg, i.p.) + Berberine (10 mg/kg, i.p.). (D) TUNEL assay determined cell apoptosis in the tumor tissues from the mice after treatment with DDP (3 mg/kg, i.p.), berberine (10 mg/kg, i.p.) or DDP (3 mg/kg, i.p.) + Berberine (10 mg/kg, i.p.). * p
    Figure Legend Snippet: Berberine sensitizes DDP-resistance gastric cancer cells to cisplatin treatment in vivo . (A) In vivo tumor growth of SGC-7901/DDP cells in the nude mice after treatment with DDP (3 mg/kg, i.p.), berberine (10 mg/kg, i.p.) or DDP (3 mg/kg, i.p.) + Berberine (10 mg/kg, i.p.). (B) Tumor weight dissected from the nude mice after treatment with DDP (3 mg/kg, i.p.), berberine (10 mg/kg, i.p.) or DDP (3 mg/kg, i.p.) + Berberine (10 mg/kg, i.p.). (C) Immunostaining of Ki-67 in the tumor tissues from the mice after treatment with DDP (3 mg/kg, i.p.), berberine (10 mg/kg, i.p.) or DDP (3 mg/kg, i.p.) + Berberine (10 mg/kg, i.p.). (D) TUNEL assay determined cell apoptosis in the tumor tissues from the mice after treatment with DDP (3 mg/kg, i.p.), berberine (10 mg/kg, i.p.) or DDP (3 mg/kg, i.p.) + Berberine (10 mg/kg, i.p.). * p

    Techniques Used: In Vivo, Mouse Assay, Immunostaining, TUNEL Assay

    29) Product Images from "Patient‐Derived Organoids Can Guide Personalized‐Therapies for Patients with Advanced Breast Cancer, Patient‐Derived Organoids Can Guide Personalized‐Therapies for Patients with Advanced Breast Cancer"

    Article Title: Patient‐Derived Organoids Can Guide Personalized‐Therapies for Patients with Advanced Breast Cancer, Patient‐Derived Organoids Can Guide Personalized‐Therapies for Patients with Advanced Breast Cancer

    Journal: Advanced Science

    doi: 10.1002/advs.202101176

    Establishing a biobank of breast cancer organoids for preclinical study. A) Isolation efficiency rate of PDOs from total, drug‐treated, treatment‐naïve, frozen, and fresh samples. B) Bright‐field microscopy images showing the representative phenotypes of breast cancer organoids. The left two images show cystic organoids (PDO023 and PDO062), the middle two images represent solid organoids (PDO105 and PDO118), the right top image has a grape‐like morphology (PDO058), and the right bottom image displays the morphology as a flower (PDO082). Scale bar: 200 µm. C) Histological and immunohistochemical images showing the organization structure and status of proliferation marker (Ki‐67) and breast cancer‐related markers (ER, PR, and HER2) in primary tumors and organoid lines. Scale bar: 50 µm. P117 and P111 represent tumor tissue, and PDO117 and PDO111 represent organoids.
    Figure Legend Snippet: Establishing a biobank of breast cancer organoids for preclinical study. A) Isolation efficiency rate of PDOs from total, drug‐treated, treatment‐naïve, frozen, and fresh samples. B) Bright‐field microscopy images showing the representative phenotypes of breast cancer organoids. The left two images show cystic organoids (PDO023 and PDO062), the middle two images represent solid organoids (PDO105 and PDO118), the right top image has a grape‐like morphology (PDO058), and the right bottom image displays the morphology as a flower (PDO082). Scale bar: 200 µm. C) Histological and immunohistochemical images showing the organization structure and status of proliferation marker (Ki‐67) and breast cancer‐related markers (ER, PR, and HER2) in primary tumors and organoid lines. Scale bar: 50 µm. P117 and P111 represent tumor tissue, and PDO117 and PDO111 represent organoids.

    Techniques Used: Isolation, Microscopy, Immunohistochemistry, Marker

    30) Product Images from "Enhanced Sensitivity to NVP-BEZ235 by Inhibition of p62/SQSTM1 in Human Bladder Cancer KoTCC-1 Cells Both In Vitro and In Vivo"

    Article Title: Enhanced Sensitivity to NVP-BEZ235 by Inhibition of p62/SQSTM1 in Human Bladder Cancer KoTCC-1 Cells Both In Vitro and In Vivo

    Journal: In Vivo

    doi: 10.21873/invivo.11868

    Histopathological study of KoTCC-1 tumors after treatment with NVP-BEZ235. In vivo subcutaneous tumors were harvested from nude mice undergoing treatment with NVP-BEZ235 or vehicle for 4 weeks according to the schedule described in Figure 3. Sections from each tumor tissue were examined by immunohistochemical staining with antibodies against Ki-67 and p62, and TUNEL staining.
    Figure Legend Snippet: Histopathological study of KoTCC-1 tumors after treatment with NVP-BEZ235. In vivo subcutaneous tumors were harvested from nude mice undergoing treatment with NVP-BEZ235 or vehicle for 4 weeks according to the schedule described in Figure 3. Sections from each tumor tissue were examined by immunohistochemical staining with antibodies against Ki-67 and p62, and TUNEL staining.

    Techniques Used: In Vivo, Mouse Assay, Immunohistochemistry, Staining, TUNEL Assay

    31) Product Images from "MicroRNA-346 inhibits the growth of glioma by directly targeting NFIB"

    Article Title: MicroRNA-346 inhibits the growth of glioma by directly targeting NFIB

    Journal: Cancer Cell International

    doi: 10.1186/s12935-019-1017-5

    miR-346 overexpression suppresses glioma growth in vivo. a Tumor growth curves after subcutaneous injection of nude mice with U87 cells stably expressing miR-NC or miR-346 (n = 10). Tumor volumes were measured every 3 days from days 3 to 30. b–d Analysis of miR-NC- and miR-346-expressing U87 tumors on day 30 after injection: representative tumor images ( b ); tumor weights ( c ); immunohistochemical staining of NFIB and Ki-67 ( d ); ***P
    Figure Legend Snippet: miR-346 overexpression suppresses glioma growth in vivo. a Tumor growth curves after subcutaneous injection of nude mice with U87 cells stably expressing miR-NC or miR-346 (n = 10). Tumor volumes were measured every 3 days from days 3 to 30. b–d Analysis of miR-NC- and miR-346-expressing U87 tumors on day 30 after injection: representative tumor images ( b ); tumor weights ( c ); immunohistochemical staining of NFIB and Ki-67 ( d ); ***P

    Techniques Used: Over Expression, In Vivo, Injection, Mouse Assay, Stable Transfection, Expressing, Immunohistochemistry, Staining

    32) Product Images from "NF2 deficiency accelerates neointima hyperplasia following vascular injury via promoting YAP-TEAD1 interaction in vascular smooth muscle cells"

    Article Title: NF2 deficiency accelerates neointima hyperplasia following vascular injury via promoting YAP-TEAD1 interaction in vascular smooth muscle cells

    Journal: Aging (Albany NY)

    doi: 10.18632/aging.103240

    VSMC proliferation and migration in vitro is elevated after NF2 knockdown. ( A ) The relative protein expression levels of p-NF2 Ser518 and NF2 were determined by immunoblotting in VSMC after 0, 24 and 48 h of physiological saline or PDGF-BB (30 ng/mL) treatment (n=5). ( B ) VSMC isolated from WT or Nf2 -/- mice was stained with SM α-actin (red), Ki-67 (green) and DAPI (blue) after 48 h of physiological saline or PDGF-BB (30 ng/mL) treatment. Representative images (left) and corresponding quantification of Ki-67 positive VSMC (right) were shown (n=5). Magnification 400×. ( C ) Migration of VSMC isolated from WT and Nf2 -/- mice after 24 h of physiological saline or PDGF-BB (30 ng/mL) treatment was measured via wound healing assay. Representative images (upper panel) and corresponding quantification of healing rates (lower panel) were shown (n=5). Magnification 100×. ( D ) VSMC isolated from WT or Nf2 -/- mice after 8 h of physiological saline or PDGF-BB (30 ng/mL) treatment was assessed by transwell assay. Representative images (upper panel) and corresponding quantification of migration cells (lower panel) were shown (n=5). Magnification 100×. Data are shown as mean ± S.D. ** P
    Figure Legend Snippet: VSMC proliferation and migration in vitro is elevated after NF2 knockdown. ( A ) The relative protein expression levels of p-NF2 Ser518 and NF2 were determined by immunoblotting in VSMC after 0, 24 and 48 h of physiological saline or PDGF-BB (30 ng/mL) treatment (n=5). ( B ) VSMC isolated from WT or Nf2 -/- mice was stained with SM α-actin (red), Ki-67 (green) and DAPI (blue) after 48 h of physiological saline or PDGF-BB (30 ng/mL) treatment. Representative images (left) and corresponding quantification of Ki-67 positive VSMC (right) were shown (n=5). Magnification 400×. ( C ) Migration of VSMC isolated from WT and Nf2 -/- mice after 24 h of physiological saline or PDGF-BB (30 ng/mL) treatment was measured via wound healing assay. Representative images (upper panel) and corresponding quantification of healing rates (lower panel) were shown (n=5). Magnification 100×. ( D ) VSMC isolated from WT or Nf2 -/- mice after 8 h of physiological saline or PDGF-BB (30 ng/mL) treatment was assessed by transwell assay. Representative images (upper panel) and corresponding quantification of migration cells (lower panel) were shown (n=5). Magnification 100×. Data are shown as mean ± S.D. ** P

    Techniques Used: Migration, In Vitro, Expressing, Isolation, Mouse Assay, Staining, Wound Healing Assay, Transwell Assay

    YAP is required for NF2 knockdown-mediated neointima hyperplasia after vascular injury. WT and Nf2 -/- mice received injection of shCon, shYap, Ad-Con and Ad-Yap into the injured left common carotid artery via the external carotid artery immediately after injury and then incubated for 30 min. The mice subsequently received intravenous injection of these adenovirus via tail vein at 7, 14, 21 days after injury. ( A ) The relative protein expression levels of p-YAP Ser127 and YAP were determined by immunoblotting in arteries of WT and Nf2 -/- mice at day 28 after vascular injury (n=5). ( B ) Representative H E staining of carotid arteries from WT or Nf2 -/- mice treated as above mentioned (left) and corresponding quantification for ratio of intima/media (right) were shown (n=5). Magnification 200×. ( C ) Immunohistochemistry staining of Ki-67 (brown) in sections of carotid arteries from WT or Nf2 -/- mice treated as above mentioned (left) and corresponding quantification for Ki-67-positive cells within neointima (right) were shown (n=5). Magnification 200×. Data are shown as mean ± S.D. * P
    Figure Legend Snippet: YAP is required for NF2 knockdown-mediated neointima hyperplasia after vascular injury. WT and Nf2 -/- mice received injection of shCon, shYap, Ad-Con and Ad-Yap into the injured left common carotid artery via the external carotid artery immediately after injury and then incubated for 30 min. The mice subsequently received intravenous injection of these adenovirus via tail vein at 7, 14, 21 days after injury. ( A ) The relative protein expression levels of p-YAP Ser127 and YAP were determined by immunoblotting in arteries of WT and Nf2 -/- mice at day 28 after vascular injury (n=5). ( B ) Representative H E staining of carotid arteries from WT or Nf2 -/- mice treated as above mentioned (left) and corresponding quantification for ratio of intima/media (right) were shown (n=5). Magnification 200×. ( C ) Immunohistochemistry staining of Ki-67 (brown) in sections of carotid arteries from WT or Nf2 -/- mice treated as above mentioned (left) and corresponding quantification for Ki-67-positive cells within neointima (right) were shown (n=5). Magnification 200×. Data are shown as mean ± S.D. * P

    Techniques Used: Mouse Assay, Injection, Incubation, Expressing, Staining, Immunohistochemistry

    NF2 knockdown accelerates PDGF-BB-induced VSMC proliferation and migration in a YAP-dependent manner. VSMC isolated from WT or Nf2 -/- mice was transfected by shCon, shYap, Ad-Con and Ad-Yap. Then the VSMC received 48 h of physiological saline or PDGF-BB (30 ng/mL) treatment. ( A ) The relative protein expression levels of p-YAP Ser127 and YAP were determined by immunoblotting in VSMC treated as above mentioned (n=5). ( B ) VSMC treated as above mentioned was stained with SM α-actin (red), Ki-67 (green) and DAPI (blue). Representative images (left) and corresponding quantification of Ki-67-positive VSMC (right) were shown (n=5). Magnification 400×. ( C ) VSMC treated as above mentioned was assessed by transwell assay. Representative images (left) and corresponding quantification of migration cells (right) were shown (n=5). Magnification 100×. Data are shown as mean ± S.D. * P
    Figure Legend Snippet: NF2 knockdown accelerates PDGF-BB-induced VSMC proliferation and migration in a YAP-dependent manner. VSMC isolated from WT or Nf2 -/- mice was transfected by shCon, shYap, Ad-Con and Ad-Yap. Then the VSMC received 48 h of physiological saline or PDGF-BB (30 ng/mL) treatment. ( A ) The relative protein expression levels of p-YAP Ser127 and YAP were determined by immunoblotting in VSMC treated as above mentioned (n=5). ( B ) VSMC treated as above mentioned was stained with SM α-actin (red), Ki-67 (green) and DAPI (blue). Representative images (left) and corresponding quantification of Ki-67-positive VSMC (right) were shown (n=5). Magnification 400×. ( C ) VSMC treated as above mentioned was assessed by transwell assay. Representative images (left) and corresponding quantification of migration cells (right) were shown (n=5). Magnification 100×. Data are shown as mean ± S.D. * P

    Techniques Used: Migration, Isolation, Mouse Assay, Transfection, Expressing, Staining, Transwell Assay

    NF2 knockdown causes increased VSMC proliferation and migration induced by PDGF-BB via inducing YAP-TEAD1 interaction. ( A ) VSMC isolated from WT or Nf2 -/- mice after 48 h of physiological saline or PDGF-BB (30 ng/mL) treatment was subjected to immunoprecipitation using anti-YAP antibody or control IgG. Inputs and immunocomplexes were analyzed by immunoblotting. VSMC isolated from WT and Nf2 -/- mice was transfected with control siRNA, Teadi or Ad-Con, Ad-Yap and then treated by physiological saline or PDGF-BB (30 ng/mL) for 48 h. ( B ) VSMC treated as above mentioned was stained with SM α-actin (red), Ki-67 (green) and DAPI (blue). Representative images (left) and corresponding quantification of Ki-67-positive VSMC (right) were shown (n=5). Magnification 400×. ( C ) VSMC treated as above mentioned was assessed by transwell assay. Representative images (left) and corresponding quantification of migration cells (right) were shown (n=5). Magnification 100×. Data are shown as mean ± S.D. * P
    Figure Legend Snippet: NF2 knockdown causes increased VSMC proliferation and migration induced by PDGF-BB via inducing YAP-TEAD1 interaction. ( A ) VSMC isolated from WT or Nf2 -/- mice after 48 h of physiological saline or PDGF-BB (30 ng/mL) treatment was subjected to immunoprecipitation using anti-YAP antibody or control IgG. Inputs and immunocomplexes were analyzed by immunoblotting. VSMC isolated from WT and Nf2 -/- mice was transfected with control siRNA, Teadi or Ad-Con, Ad-Yap and then treated by physiological saline or PDGF-BB (30 ng/mL) for 48 h. ( B ) VSMC treated as above mentioned was stained with SM α-actin (red), Ki-67 (green) and DAPI (blue). Representative images (left) and corresponding quantification of Ki-67-positive VSMC (right) were shown (n=5). Magnification 400×. ( C ) VSMC treated as above mentioned was assessed by transwell assay. Representative images (left) and corresponding quantification of migration cells (right) were shown (n=5). Magnification 100×. Data are shown as mean ± S.D. * P

    Techniques Used: Migration, Isolation, Mouse Assay, Immunoprecipitation, Transfection, Staining, Transwell Assay

    NF2 knockdown enhances neointima hyperplasia after vascular injury. WT or Nf2 -/- mice received sham operation or wire injury in common carotid artery. ( A ) The relative protein levels of p-NF2 Ser518 and NF2 in common carotid arteries from C57BL/6J mice at day 7, 14 and 28 after injury were analyzed by immunoblotting (n=5). ( B ) The relative mRNA (n=5) level of Nf2 in common carotid arteries from WT or Nf2 -/- mice. ( C ) The relative protein (n=3) levels of p-NF2 Ser518 and NF2 in common carotid arteries from WT or Nf2 -/- mice. ( D ) Representative H E staining of carotid arteries from WT or Nf2 -/- mice at day 28 after sham operation or wire injury (left) and corresponding quantification for ratio of intima/media (right) were shown (n=6). Magnification 200×. ( E ) Immunohistochemistry staining of Ki-67 (brown) in sections of carotid arteries from WT or Nf2 -/- mice at day 28 after sham operation or wire injury (left) and corresponding quantification for Ki-67 positive cells within neointima (right) were shown (n=6). Magnification 200×. Data are shown as mean ± S.D. * P
    Figure Legend Snippet: NF2 knockdown enhances neointima hyperplasia after vascular injury. WT or Nf2 -/- mice received sham operation or wire injury in common carotid artery. ( A ) The relative protein levels of p-NF2 Ser518 and NF2 in common carotid arteries from C57BL/6J mice at day 7, 14 and 28 after injury were analyzed by immunoblotting (n=5). ( B ) The relative mRNA (n=5) level of Nf2 in common carotid arteries from WT or Nf2 -/- mice. ( C ) The relative protein (n=3) levels of p-NF2 Ser518 and NF2 in common carotid arteries from WT or Nf2 -/- mice. ( D ) Representative H E staining of carotid arteries from WT or Nf2 -/- mice at day 28 after sham operation or wire injury (left) and corresponding quantification for ratio of intima/media (right) were shown (n=6). Magnification 200×. ( E ) Immunohistochemistry staining of Ki-67 (brown) in sections of carotid arteries from WT or Nf2 -/- mice at day 28 after sham operation or wire injury (left) and corresponding quantification for Ki-67 positive cells within neointima (right) were shown (n=6). Magnification 200×. Data are shown as mean ± S.D. * P

    Techniques Used: Mouse Assay, Staining, Immunohistochemistry

    33) Product Images from "Serial transplantation unmasks galectin-9 contribution to tumor immune escape in the MB49 murine model"

    Article Title: Serial transplantation unmasks galectin-9 contribution to tumor immune escape in the MB49 murine model

    Journal: Scientific Reports

    doi: 10.1038/s41598-021-84270-1

    In gal-9-KO tumors, late stages of tumor growth reduction are associated with an increase in T-cells infiltrating tumor nodules. ( A ) Low magnification of CD45 staining on sections of WT and gal-9-KO tumors at cycles 2, 3 and 4 (tumors derived from clones # 116 and 345, respectively). At cycle 2, CD45 staining was detected almost exclusively in peri-nodular septa. However, for gal-9-KO tumors, at cycle 3 and even more at cycle 4, CD45 was becoming more and more abundant inside the tumor nodules. ( B ) High magnification of CD45, Ki-67, CD4 and CD8 staining on serial sections of a WT-Ctrl tumor (#116) and a gal-9-KO tumor (#345) at cycle 4. ( C ) Quantitative assessment of CD45, CD4 and CD8 staining on serial sections of tumors collected at cycles 2, 3 and 4 of tumor growth. Digitalization was performed in large Regions of Interest (ROIs) covering in as much as possible the whole tumor sections and excluding areas with absence or very low levels of Ki-67 staining, including peri-nodular septa. Therefore these ROIs were covering mainly the internal parts of the tumor nodules. Ratios of CD45, CD4 or CD8 to Ki-67 staining densities were acquired in these ROIs and plotted for each tumor growth cycles. Comparisons of mean ratios obtained for WT and KO tumors were subjected to Mann–Whitney tests for assessment of statistical significance.
    Figure Legend Snippet: In gal-9-KO tumors, late stages of tumor growth reduction are associated with an increase in T-cells infiltrating tumor nodules. ( A ) Low magnification of CD45 staining on sections of WT and gal-9-KO tumors at cycles 2, 3 and 4 (tumors derived from clones # 116 and 345, respectively). At cycle 2, CD45 staining was detected almost exclusively in peri-nodular septa. However, for gal-9-KO tumors, at cycle 3 and even more at cycle 4, CD45 was becoming more and more abundant inside the tumor nodules. ( B ) High magnification of CD45, Ki-67, CD4 and CD8 staining on serial sections of a WT-Ctrl tumor (#116) and a gal-9-KO tumor (#345) at cycle 4. ( C ) Quantitative assessment of CD45, CD4 and CD8 staining on serial sections of tumors collected at cycles 2, 3 and 4 of tumor growth. Digitalization was performed in large Regions of Interest (ROIs) covering in as much as possible the whole tumor sections and excluding areas with absence or very low levels of Ki-67 staining, including peri-nodular septa. Therefore these ROIs were covering mainly the internal parts of the tumor nodules. Ratios of CD45, CD4 or CD8 to Ki-67 staining densities were acquired in these ROIs and plotted for each tumor growth cycles. Comparisons of mean ratios obtained for WT and KO tumors were subjected to Mann–Whitney tests for assessment of statistical significance.

    Techniques Used: Staining, Derivative Assay, Clone Assay, MANN-WHITNEY

    34) Product Images from "Yes-associated protein (YAP) mediates adaptive cardiac hypertrophy in response to pressure overload"

    Article Title: Yes-associated protein (YAP) mediates adaptive cardiac hypertrophy in response to pressure overload

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.RA118.006123

    Heterozygous down-regulation of YAP inhibits CM cell cycle re-entry 7 days after TAC. WT and YAP-CHKO mice were subjected to either TAC or sham operation for 7 days. A, heart sections were stained with anti-Ki-67 ( green ), anti-troponin T ( red ), and DAPI ( blue ). The arrow indicates a Ki-67–positive CM. B, quantification of Ki-67–positive CMs (%) detected in WT and YAP-CHKO mouse hearts. n = 4. Values are mean ± S.D. *, p
    Figure Legend Snippet: Heterozygous down-regulation of YAP inhibits CM cell cycle re-entry 7 days after TAC. WT and YAP-CHKO mice were subjected to either TAC or sham operation for 7 days. A, heart sections were stained with anti-Ki-67 ( green ), anti-troponin T ( red ), and DAPI ( blue ). The arrow indicates a Ki-67–positive CM. B, quantification of Ki-67–positive CMs (%) detected in WT and YAP-CHKO mouse hearts. n = 4. Values are mean ± S.D. *, p

    Techniques Used: Mouse Assay, Staining

    35) Product Images from "Circular RNA CircEYA3 induces energy production to promote pancreatic ductal adenocarcinoma progression through the miR-1294/c-Myc axis"

    Article Title: Circular RNA CircEYA3 induces energy production to promote pancreatic ductal adenocarcinoma progression through the miR-1294/c-Myc axis

    Journal: Molecular Cancer

    doi: 10.1186/s12943-021-01400-z

    Knockdown of circEYA3 suppresses tumor growth in vivo. A. Stably transfected PANC-1 cells from different groups were inoculated into BALB/c nude mice to establish subcutaneous xenograft tumors ( n = 5 mice/group). Representative images of tumor-bearing mice. In addition, tumor volumes were monitored weekly. B . The excised tumors were photographed and weighed. C . The relative expression levels of circEYA3, miR-1294 and c-Myc in subcutaneous tumor tissues were determined by qRT-PCR. D . The c-Myc, E-cadherin, N-cadherin, Vimentin, Snail, Bax, cleaved caspase-3 protein levels in tumours from different groups were determined by western blot analysis. E . IHC staining showed the relative levels of c-Myc, E-cadherin, N-cadherin, Bax, cleaved caspase-3, and Ki-67 in tumours from different groups. Scale bar, 50 μm. * P
    Figure Legend Snippet: Knockdown of circEYA3 suppresses tumor growth in vivo. A. Stably transfected PANC-1 cells from different groups were inoculated into BALB/c nude mice to establish subcutaneous xenograft tumors ( n = 5 mice/group). Representative images of tumor-bearing mice. In addition, tumor volumes were monitored weekly. B . The excised tumors were photographed and weighed. C . The relative expression levels of circEYA3, miR-1294 and c-Myc in subcutaneous tumor tissues were determined by qRT-PCR. D . The c-Myc, E-cadherin, N-cadherin, Vimentin, Snail, Bax, cleaved caspase-3 protein levels in tumours from different groups were determined by western blot analysis. E . IHC staining showed the relative levels of c-Myc, E-cadherin, N-cadherin, Bax, cleaved caspase-3, and Ki-67 in tumours from different groups. Scale bar, 50 μm. * P

    Techniques Used: In Vivo, Stable Transfection, Transfection, Mouse Assay, Expressing, Quantitative RT-PCR, Western Blot, Immunohistochemistry, Staining

    36) Product Images from "AKR1C2 acts as a targetable oncogene in esophageal squamous cell carcinoma via activating PI3K/AKT signaling pathway, et al. AKR1C2 acts as a targetable oncogene in esophageal squamous cell carcinoma via activating PI3K/AKT signaling pathway"

    Article Title: AKR1C2 acts as a targetable oncogene in esophageal squamous cell carcinoma via activating PI3K/AKT signaling pathway, et al. AKR1C2 acts as a targetable oncogene in esophageal squamous cell carcinoma via activating PI3K/AKT signaling pathway

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.15604

    PI3K/AKT signalling pathway was regulated by AKR1C2. A, Three pairs of matched tumour/normal tissues were performed with RNA‐sequencing and the KEGG results were shown, and the PI3K/AKT signalling pathway was circled with a rectangle. B, The pAKT protein level was detected by Western blotting in six pairs of ESCC tissues and corresponding adjacent normal tissues. C, The KYSE30 cell was transfected with an empty vector or AKR1C2 plasmid for 72 h, mRNA sequencing analysis was performed, and the KEGG results were shown, the PI3K/AKT signalling pathway and platinum drug resistance were highlighted by rectangles. D, Western blotting analysis the change of pAKT in the indicated ESCC cell lines. E, The IHC was performed to detect the AKR1C2‐mediated expression change of pAKT and Ki‐67 in the excised tumours from tumour growth models. The arrows indicated regional areas, suggesting a positive correlation between the AKR1C2, pAKT and Ki‐67. The pictures were taken at 200× original magnification. Scale bar, 50 μm. F, The correlation between AKR1C2 and pAKT expression was analysed by IHC in 47 ESCC clinical samples ( r = .5669, P
    Figure Legend Snippet: PI3K/AKT signalling pathway was regulated by AKR1C2. A, Three pairs of matched tumour/normal tissues were performed with RNA‐sequencing and the KEGG results were shown, and the PI3K/AKT signalling pathway was circled with a rectangle. B, The pAKT protein level was detected by Western blotting in six pairs of ESCC tissues and corresponding adjacent normal tissues. C, The KYSE30 cell was transfected with an empty vector or AKR1C2 plasmid for 72 h, mRNA sequencing analysis was performed, and the KEGG results were shown, the PI3K/AKT signalling pathway and platinum drug resistance were highlighted by rectangles. D, Western blotting analysis the change of pAKT in the indicated ESCC cell lines. E, The IHC was performed to detect the AKR1C2‐mediated expression change of pAKT and Ki‐67 in the excised tumours from tumour growth models. The arrows indicated regional areas, suggesting a positive correlation between the AKR1C2, pAKT and Ki‐67. The pictures were taken at 200× original magnification. Scale bar, 50 μm. F, The correlation between AKR1C2 and pAKT expression was analysed by IHC in 47 ESCC clinical samples ( r = .5669, P

    Techniques Used: RNA Sequencing Assay, Western Blot, Transfection, Plasmid Preparation, Sequencing, Immunohistochemistry, Expressing

    37) Product Images from "Antitumor activity of celastrol by inhibition of proliferation, invasion, and migration in cholangiocarcinoma via PTEN/PI3K/Akt pathway. Antitumor activity of celastrol by inhibition of proliferation, invasion, and migration in cholangiocarcinoma via PTEN/PI3K/Akt pathway"

    Article Title: Antitumor activity of celastrol by inhibition of proliferation, invasion, and migration in cholangiocarcinoma via PTEN/PI3K/Akt pathway. Antitumor activity of celastrol by inhibition of proliferation, invasion, and migration in cholangiocarcinoma via PTEN/PI3K/Akt pathway

    Journal: Cancer Medicine

    doi: 10.1002/cam4.2719

    Immunohistochemical characterization of tumor tissues. A, Immunohistochemical analyses of Ki 67, cleaved caspase 3, vimentin, p‐AKT, and PTEN. Note the proliferation activity in tissue by Ki67‐positive tumor cells, apoptosis by cleaved caspase‐3, and EMT by vimentin (200 × magnification). B, The levels of relative proteins were analyzed. * P
    Figure Legend Snippet: Immunohistochemical characterization of tumor tissues. A, Immunohistochemical analyses of Ki 67, cleaved caspase 3, vimentin, p‐AKT, and PTEN. Note the proliferation activity in tissue by Ki67‐positive tumor cells, apoptosis by cleaved caspase‐3, and EMT by vimentin (200 × magnification). B, The levels of relative proteins were analyzed. * P

    Techniques Used: Immunohistochemistry, Activity Assay

    38) Product Images from "Ramucirumab-related Oral Pyogenic Granuloma: A Report of Two Cases"

    Article Title: Ramucirumab-related Oral Pyogenic Granuloma: A Report of Two Cases

    Journal: Internal Medicine

    doi: 10.2169/internalmedicine.6650-20

    Histopathological characteristics of case 2. (a, b) Hematoxylin and Eosin staining. a: ×100, b: ×400. A large number of capillaries showing foliar compaction can be seen beneath the mucous membrane. Hemorrhaging and slight inflammatory cell infiltration can be seen in the stroma. No malignant cells are observed; the findings are consistent with those of pyogenic granuloma. (c, d) CD31 (c) and D2-40 (d) immunostaining: endothelial cells are positive for CD31 and negative for D2-40. (e) Vascular endothelial growth factor receptor-2 (VEGFR2) immunostaining. Strong staining can be seen in almost all vascular endothelial cells. (f) The Ki-67 cell proliferation marker is also frequently detected in vascular endothelial cells.
    Figure Legend Snippet: Histopathological characteristics of case 2. (a, b) Hematoxylin and Eosin staining. a: ×100, b: ×400. A large number of capillaries showing foliar compaction can be seen beneath the mucous membrane. Hemorrhaging and slight inflammatory cell infiltration can be seen in the stroma. No malignant cells are observed; the findings are consistent with those of pyogenic granuloma. (c, d) CD31 (c) and D2-40 (d) immunostaining: endothelial cells are positive for CD31 and negative for D2-40. (e) Vascular endothelial growth factor receptor-2 (VEGFR2) immunostaining. Strong staining can be seen in almost all vascular endothelial cells. (f) The Ki-67 cell proliferation marker is also frequently detected in vascular endothelial cells.

    Techniques Used: Staining, Immunostaining, Marker

    Histopathological characteristics of case 1. (a, b) Hematoxylin and Eosin staining. a: ×100, b: ×400. A large number of capillaries showing foliar compaction can be seen beneath the mucous membrane. Hemorrhaging and slight inflammatory cell infiltration can be seen in the stroma. No malignant cells are observed; the findings are consistent with those of pyogenic granuloma. (c, d) Endothelial cells positive for CD31 (c) and negative for D2-40 (d) can be seen. (e) Strong immunostaining for vascular endothelial growth factor receptor-2 (VEGFR2) can be seen in almost all vascular endothelial cells. (f) Cell proliferation marker Ki-67 is also frequently detected.
    Figure Legend Snippet: Histopathological characteristics of case 1. (a, b) Hematoxylin and Eosin staining. a: ×100, b: ×400. A large number of capillaries showing foliar compaction can be seen beneath the mucous membrane. Hemorrhaging and slight inflammatory cell infiltration can be seen in the stroma. No malignant cells are observed; the findings are consistent with those of pyogenic granuloma. (c, d) Endothelial cells positive for CD31 (c) and negative for D2-40 (d) can be seen. (e) Strong immunostaining for vascular endothelial growth factor receptor-2 (VEGFR2) can be seen in almost all vascular endothelial cells. (f) Cell proliferation marker Ki-67 is also frequently detected.

    Techniques Used: Staining, Immunostaining, Marker

    39) Product Images from "Overcoming radio-resistance in esophageal squamous cell carcinoma via hypermethylation of PIK3C3 promoter region mediated by KDM5B loss"

    Article Title: Overcoming radio-resistance in esophageal squamous cell carcinoma via hypermethylation of PIK3C3 promoter region mediated by KDM5B loss

    Journal: Journal of Radiation Research

    doi: 10.1093/jrr/rrac004

    Inhibition of KDM5B inhibits the radio-resistance of ESCC in mouse xenografts. (A) Tumor volume growth of nude mice after radiation. (B) changes in tumor weight. (C) The protein expression of PIK3C3 in tumor tissues examined using Western blot analysis. (D) Immunohistochemical assessment of the percentage of Ki-67-positive cells in tumor tissues. (E) The proportion of apoptotic cells in tumor tissues assessed using TUNEL staining. * P
    Figure Legend Snippet: Inhibition of KDM5B inhibits the radio-resistance of ESCC in mouse xenografts. (A) Tumor volume growth of nude mice after radiation. (B) changes in tumor weight. (C) The protein expression of PIK3C3 in tumor tissues examined using Western blot analysis. (D) Immunohistochemical assessment of the percentage of Ki-67-positive cells in tumor tissues. (E) The proportion of apoptotic cells in tumor tissues assessed using TUNEL staining. * P

    Techniques Used: Inhibition, Mouse Assay, Expressing, Western Blot, Immunohistochemistry, TUNEL Assay, Staining

    40) Product Images from "Bcl‐2/Bcl‐xl inhibitor APG‐1252‐M1 is a promising therapeutic strategy for gastric carcinoma, et al. Bcl‐2/Bcl‐xl inhibitor APG‐1252‐M1 is a promising therapeutic strategy for gastric carcinoma"

    Article Title: Bcl‐2/Bcl‐xl inhibitor APG‐1252‐M1 is a promising therapeutic strategy for gastric carcinoma, et al. Bcl‐2/Bcl‐xl inhibitor APG‐1252‐M1 is a promising therapeutic strategy for gastric carcinoma

    Journal: Cancer Medicine

    doi: 10.1002/cam4.3090

    APG‐1252 suppressed tumor growth in vivo. A, Tumor volumes in the four groups. B, Compared to other groups, the tumor volume in the group of APG‐1252 100 mg/kg was the smallest. C, The tumor weight in the group of APG‐1252 100 mg/kg was lightest among the four groups. D, No remarkable diversity in body weight was found among the four groups. E, The results of Western blot show the change of proteins associated with the Bcl‐2 family and DNA damage in tumor tissue of four groups (N87). F, The results of immunohistochemistry show the expression level of BCL‐2, MCL‐1, BAX, Cleaved Caspase 3, and Ki‐67 among four groups. G, Quantification of the Ki‐67 in four groups
    Figure Legend Snippet: APG‐1252 suppressed tumor growth in vivo. A, Tumor volumes in the four groups. B, Compared to other groups, the tumor volume in the group of APG‐1252 100 mg/kg was the smallest. C, The tumor weight in the group of APG‐1252 100 mg/kg was lightest among the four groups. D, No remarkable diversity in body weight was found among the four groups. E, The results of Western blot show the change of proteins associated with the Bcl‐2 family and DNA damage in tumor tissue of four groups (N87). F, The results of immunohistochemistry show the expression level of BCL‐2, MCL‐1, BAX, Cleaved Caspase 3, and Ki‐67 among four groups. G, Quantification of the Ki‐67 in four groups

    Techniques Used: In Vivo, Western Blot, Immunohistochemistry, Expressing

    APG‐1252 enhanced the antitumor effects of chemotherapeutic drugs in vivo. A, The xenograft tumor volumes of the combined group grew more slowly than did tumors in the other groups. B, The tumo volume of the combined group was the smallest. C, Compared to the other groups, the tumor weight in the combination treatment group was lightest. D, No significant differences in body weight were found among the four groups. E, F, In situ TUNEL staining showed the extent of apoptosis in a xenograft tumor model. G, We analyzed the level of BCL‐2, MCL‐1, BAX, Cleaved Caspase 3, and Ki‐67 by the method of immunohistochemistry. H, Quantification of the proliferation index (Ki‐67) in the four groups
    Figure Legend Snippet: APG‐1252 enhanced the antitumor effects of chemotherapeutic drugs in vivo. A, The xenograft tumor volumes of the combined group grew more slowly than did tumors in the other groups. B, The tumo volume of the combined group was the smallest. C, Compared to the other groups, the tumor weight in the combination treatment group was lightest. D, No significant differences in body weight were found among the four groups. E, F, In situ TUNEL staining showed the extent of apoptosis in a xenograft tumor model. G, We analyzed the level of BCL‐2, MCL‐1, BAX, Cleaved Caspase 3, and Ki‐67 by the method of immunohistochemistry. H, Quantification of the proliferation index (Ki‐67) in the four groups

    Techniques Used: In Vivo, In Situ, TUNEL Assay, Staining, Immunohistochemistry

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    Ablation of PINCH-1 inhibits lung adenocarcinoma growth in vivo. The lung of the mice (as indicated in the figure) was administrated with Ad-Cre and analyzed 16 weeks later. a Sections of the lung tissues from the mice (as specified in the figure) were analyzed by immunostaining with antibodies for <t>Ki67.</t> Bar, 20 μm. Right panels, the percentages of Ki67 positive cells in the lung tissues derived from the Kras LSL−G12D/+ ; PINCH-1 fl/fl (Kras fl/+ ; P1 fl/fl ) group were quantified and compared to those of the Kras fl/+ group (Kras fl/+ group n = 36 fields from 6 mice, Kras fl/+ ; P1 fl/fl group n = 35 fields from 6 mice, different mice in each group were coded with different colors; P
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    Cell Signaling Technology Inc ki67 d3b5 alexa fluor 488 conjugate antibody
    Proteasomal inhibition suppresses palbociclib‐induced senescence phenotype Representative maximum‐intensity projections of MCF7 cells treated with the 1 μM palbociclib and/or 7.5 nM bortezomib. Note that 7.5 nM bortezomib inhibits proteasome only partially. Fixed and permeabilized cells were stained with <t>Alexa</t> Fluor 488‐conjugated <t>Ki67</t> antibody, Alexa Fluor 647‐conjugated phospho‐Histone H2A.X (γH2AX) (pSer139) antibody, and DAPI. All images were acquired with the same magnification, and scale bar is 20 μm. Flow cytometry‐based quantifications of cell size (B), Ki67 levels (C), and pSer139 γH2AX levels (D) from the samples presented in panel (A) ( n = 4). Senescence‐associated beta‐galactosidase activity (blue staining) in MCF7 cells untreated (control) or treated with 7.5 nM bortezomib, 1 μM palbociclib, or a combination of both. Scale bar is 50 μm. Quantification of the β‐galactosidase activity levels is shown in panel (E) ( n = 4). Schematic model of palbociclib action on cell cycle and cell senescence. Data information: In panels (B–D and F), data are presented as means ± SD; each n represents an individual biological replicate. P ‐values were determined by ANOVA and two‐tailed Student's t ‐test with Holm–Sidak post hoc test; ns depicts not significant ( P > 0.05); **: P
    Ki67 D3b5 Alexa Fluor 488 Conjugate Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Ablation of PINCH-1 inhibits lung adenocarcinoma growth in vivo. The lung of the mice (as indicated in the figure) was administrated with Ad-Cre and analyzed 16 weeks later. a Sections of the lung tissues from the mice (as specified in the figure) were analyzed by immunostaining with antibodies for Ki67. Bar, 20 μm. Right panels, the percentages of Ki67 positive cells in the lung tissues derived from the Kras LSL−G12D/+ ; PINCH-1 fl/fl (Kras fl/+ ; P1 fl/fl ) group were quantified and compared to those of the Kras fl/+ group (Kras fl/+ group n = 36 fields from 6 mice, Kras fl/+ ; P1 fl/fl group n = 35 fields from 6 mice, different mice in each group were coded with different colors; P

    Journal: Nature Communications

    Article Title: PINCH-1 regulates mitochondrial dynamics to promote proline synthesis and tumor growth

    doi: 10.1038/s41467-020-18753-6

    Figure Lengend Snippet: Ablation of PINCH-1 inhibits lung adenocarcinoma growth in vivo. The lung of the mice (as indicated in the figure) was administrated with Ad-Cre and analyzed 16 weeks later. a Sections of the lung tissues from the mice (as specified in the figure) were analyzed by immunostaining with antibodies for Ki67. Bar, 20 μm. Right panels, the percentages of Ki67 positive cells in the lung tissues derived from the Kras LSL−G12D/+ ; PINCH-1 fl/fl (Kras fl/+ ; P1 fl/fl ) group were quantified and compared to those of the Kras fl/+ group (Kras fl/+ group n = 36 fields from 6 mice, Kras fl/+ ; P1 fl/fl group n = 35 fields from 6 mice, different mice in each group were coded with different colors; P

    Article Snippet: Immunohistochemistry was performed using the MaxVisionTM HRP-Polymer anti-Rabbit IHC Kit (MXB biotechnologies) with rabbit antibodies against PINCH-1 (Abcam, ab108609,1:800), PYCR1 (Proteintech,13108-1-AP,1:800), DRP1 (Proteintech,12957-1-AP,1:800), Ki67 (CST,12202P, 1:1000) or collagen 1A1 (Novus,NB600-408).

    Techniques: In Vivo, Mouse Assay, Immunostaining, Derivative Assay

    PINCH-1 regulates mitochondrial fragmentation and A549 cancer cell proliferation. PINCH-1 KO (P1KO) A549 cells were infected with lentiviral vectors encoding 3xFLAG-tagged PINCH-1 (3f-P1), or only 3xFLAG vector (3 f) for 3 days. a Cells (as indicated) were analyzed by Western blotting with antibodies recognizing PINCH-1 (P1) and tubulin. The samples were derived from the same experiment and the blots were processed in parallel. b The numbers of live cells in each well at different time points (as indicated) were analyzed using trypan blue exclusion assay as described in the “Methods” ( b , n = 3). c The relative level of mtDNA in the PINCH-1 KO A549 cells was analyzed by RT-PCR as described in the “Methods” and compared to that of wild type A549 cells (normalized to 1; n = 5; P = 0.0054). d The cells were stained with DAPI (blue) and antibody for Ki67 (purple). Bar, 25 μm. The percentages of Ki67-positive cells were quantified (right, A549 or P1KO + 3f n = 20 fields, P1KO or P1KO + 3f-P1 n = 19 fields; A549 vs P1KO P

    Journal: Nature Communications

    Article Title: PINCH-1 regulates mitochondrial dynamics to promote proline synthesis and tumor growth

    doi: 10.1038/s41467-020-18753-6

    Figure Lengend Snippet: PINCH-1 regulates mitochondrial fragmentation and A549 cancer cell proliferation. PINCH-1 KO (P1KO) A549 cells were infected with lentiviral vectors encoding 3xFLAG-tagged PINCH-1 (3f-P1), or only 3xFLAG vector (3 f) for 3 days. a Cells (as indicated) were analyzed by Western blotting with antibodies recognizing PINCH-1 (P1) and tubulin. The samples were derived from the same experiment and the blots were processed in parallel. b The numbers of live cells in each well at different time points (as indicated) were analyzed using trypan blue exclusion assay as described in the “Methods” ( b , n = 3). c The relative level of mtDNA in the PINCH-1 KO A549 cells was analyzed by RT-PCR as described in the “Methods” and compared to that of wild type A549 cells (normalized to 1; n = 5; P = 0.0054). d The cells were stained with DAPI (blue) and antibody for Ki67 (purple). Bar, 25 μm. The percentages of Ki67-positive cells were quantified (right, A549 or P1KO + 3f n = 20 fields, P1KO or P1KO + 3f-P1 n = 19 fields; A549 vs P1KO P

    Article Snippet: Immunohistochemistry was performed using the MaxVisionTM HRP-Polymer anti-Rabbit IHC Kit (MXB biotechnologies) with rabbit antibodies against PINCH-1 (Abcam, ab108609,1:800), PYCR1 (Proteintech,13108-1-AP,1:800), DRP1 (Proteintech,12957-1-AP,1:800), Ki67 (CST,12202P, 1:1000) or collagen 1A1 (Novus,NB600-408).

    Techniques: Infection, Plasmid Preparation, Western Blot, Derivative Assay, Trypan Blue Exclusion Assay, Reverse Transcription Polymerase Chain Reaction, Staining

    Ki67 + staining at the inoculation site of murine Gl261 gliomas ( A ). Scale bar, 200μm. Tumors at day 21 post-inoculation showed signs of hypoxia/necrosis ( B ). Scale bar, 500μm. Quantitation of five high power fields for each murine brain (N=12 per time point; C ). Data are expressed as mean ± SEM per high power field. a p

    Journal: bioRxiv

    Article Title: Temporal and spatial modulation of the immune response of the murine Gl261 glioma tumor microenvironment

    doi: 10.1101/858894

    Figure Lengend Snippet: Ki67 + staining at the inoculation site of murine Gl261 gliomas ( A ). Scale bar, 200μm. Tumors at day 21 post-inoculation showed signs of hypoxia/necrosis ( B ). Scale bar, 500μm. Quantitation of five high power fields for each murine brain (N=12 per time point; C ). Data are expressed as mean ± SEM per high power field. a p

    Article Snippet: 2.4 Multiplex fluorescent immunohistochemistrySections were sequentially stained using the OPAL polymer anti-rabbit HRP (PerkinElmer) or ImmPRESS™ HRP goat anti-rat IgG polymer (MP-7404; Vector Labs) with the following primary antibodies for 1 hour at room temperature; Panel 1: CD3 (0.3μg/ml; A045201; DAKO), CD4 (0.31μg/ml; ab183685; Abcam), CD8 (0.50μg/ml; ab203035; Abcam), FoxP3 (0.05μg/ml; 12653S; Cell Signaling Technologies), CD161 (0.031μg/ml; ab234107; Abcam), and Ki67 (0.084μg/ml; 12202S; Cell Signaling Technologies); Panel 2: ARG1 (0.125μg/ml; ab91279; Abcam), iNOS (8μg/ml; ab3523; Abcam), F4/80 (0.22μg/ml; 70076S; Abcam), TMEM119 (0.076μg/ml; ab209064; Abcam), CD19 (0.02μg/ml; 90176S; Cell Signaling Technologies), and Ki67 (0.084μg/ml; 12202S;Cell Signaling Technologies); Panel 3: Ly6C (0.10μg/ml; ab15627), Ly6G (0.25μg/ml; ab25377; Abcam), CD11b (0.085μg/ml; ab133357; Abcam), F4/80 (0.22μg/ml; 70076S; Cell Signaling Technologies), GFAP (1.45μg/ml; Z033401-2; DAKO) and Ki67 (0.084μg/ml; 12202S;Cell Signaling Technologies).

    Techniques: Staining, Quantitation Assay

    Release of gal‐encapsulated fluorophores in xenografts GalNP beads are based on a mesoporous silica scaffold (MCM‐41) that can be loaded with different cargoes encapsulated by a coat of 6‐mer β(1,4)‐galacto‐oligosaccharides. Cellular uptake of the GalNP beads occurs via endocytosis and, after fusion with lysosomal vesicles, the beads are released by exocytosis. The high lysosomal β‐galactosidase activity of senescent cells allows a preferential release of the cargo by a β‐galactosidase‐mediated hydrolysis of the cap. SK‐MEL‐103 melanoma cells were treated with palbociclib (1 μM) for 1 week, and senescence induction was assessed by SAβgal staining. Next, cultures were exposed to GalNP(rho) (50 μg/ml, for 16 h). Pictures show representative images illustrating rhodamine release by confocal microscopy. Cells were co‐stained with Calcein, and nuclei were stained with Hoechst. Graphs to the right show the rhodamine intensity relative to cell surface in senescent cells and non‐senescent (control) cells. Each assay was repeated at least three times with similar results. Scale bar: 50 μm. Subcutaneous tumor xenografts of SK‐MEL‐103 melanoma cells in athymic female nude mice. Upon tumor formation, mice were treated daily with palbociclib (oral gavage, 100 mg/kg) during 7 days. The left panel picture shows representative whole tissue portions of tumors after SAβGal staining. The right panel shows sections of control and palbociclib‐treated tumors processed for SAβGal staining, and Ki67 and phosphorylated Rb (p‐Rb) immunohistochemistry. This experiment has been repeated at least two times with similar results. Scale bar: 50 μm. Mice bearing SK‐MEL‐103 xenografts, control or treated with palbociclib for 7 days, as in (C), were tail vein injected with 200 μl of a solution containing GalNP(rho) (4 mg/ml). At 6 h post‐injection, mice were sacrificed, tumors were collected, and fluorescence was analyzed by an IVIS spectrum imaging system. The graph indicates the average difference in tumor radiance between GalNP‐injected control and palbociclib‐treated groups. The inset shows the absolute values of radiance (p/s/cm 2 /sr × 10 6 ) for each group. The corresponding differences are highlighted in black or red. Values are expressed as mean ± SD, and statistical significance was assessed by the two‐tailed Student's t ‐test.

    Journal: EMBO Molecular Medicine

    Article Title: A versatile drug delivery system targeting senescent cells

    doi: 10.15252/emmm.201809355

    Figure Lengend Snippet: Release of gal‐encapsulated fluorophores in xenografts GalNP beads are based on a mesoporous silica scaffold (MCM‐41) that can be loaded with different cargoes encapsulated by a coat of 6‐mer β(1,4)‐galacto‐oligosaccharides. Cellular uptake of the GalNP beads occurs via endocytosis and, after fusion with lysosomal vesicles, the beads are released by exocytosis. The high lysosomal β‐galactosidase activity of senescent cells allows a preferential release of the cargo by a β‐galactosidase‐mediated hydrolysis of the cap. SK‐MEL‐103 melanoma cells were treated with palbociclib (1 μM) for 1 week, and senescence induction was assessed by SAβgal staining. Next, cultures were exposed to GalNP(rho) (50 μg/ml, for 16 h). Pictures show representative images illustrating rhodamine release by confocal microscopy. Cells were co‐stained with Calcein, and nuclei were stained with Hoechst. Graphs to the right show the rhodamine intensity relative to cell surface in senescent cells and non‐senescent (control) cells. Each assay was repeated at least three times with similar results. Scale bar: 50 μm. Subcutaneous tumor xenografts of SK‐MEL‐103 melanoma cells in athymic female nude mice. Upon tumor formation, mice were treated daily with palbociclib (oral gavage, 100 mg/kg) during 7 days. The left panel picture shows representative whole tissue portions of tumors after SAβGal staining. The right panel shows sections of control and palbociclib‐treated tumors processed for SAβGal staining, and Ki67 and phosphorylated Rb (p‐Rb) immunohistochemistry. This experiment has been repeated at least two times with similar results. Scale bar: 50 μm. Mice bearing SK‐MEL‐103 xenografts, control or treated with palbociclib for 7 days, as in (C), were tail vein injected with 200 μl of a solution containing GalNP(rho) (4 mg/ml). At 6 h post‐injection, mice were sacrificed, tumors were collected, and fluorescence was analyzed by an IVIS spectrum imaging system. The graph indicates the average difference in tumor radiance between GalNP‐injected control and palbociclib‐treated groups. The inset shows the absolute values of radiance (p/s/cm 2 /sr × 10 6 ) for each group. The corresponding differences are highlighted in black or red. Values are expressed as mean ± SD, and statistical significance was assessed by the two‐tailed Student's t ‐test.

    Article Snippet: Antigen retrieval was first performed with high pH buffer (CC1m, Roche), endogenous peroxidase was blocked, and slides were then incubated with the appropriate primary antibodies as detailed: Ki67 (Master Diagnostica, #0003110QD), phosphorylated Rb (Ser807/811) (Cell Signalling Technology, #9308).

    Techniques: Activity Assay, Staining, Confocal Microscopy, Mouse Assay, Immunohistochemistry, Injection, Fluorescence, Imaging, Two Tailed Test

    Proteasomal inhibition suppresses palbociclib‐induced senescence phenotype Representative maximum‐intensity projections of MCF7 cells treated with the 1 μM palbociclib and/or 7.5 nM bortezomib. Note that 7.5 nM bortezomib inhibits proteasome only partially. Fixed and permeabilized cells were stained with Alexa Fluor 488‐conjugated Ki67 antibody, Alexa Fluor 647‐conjugated phospho‐Histone H2A.X (γH2AX) (pSer139) antibody, and DAPI. All images were acquired with the same magnification, and scale bar is 20 μm. Flow cytometry‐based quantifications of cell size (B), Ki67 levels (C), and pSer139 γH2AX levels (D) from the samples presented in panel (A) ( n = 4). Senescence‐associated beta‐galactosidase activity (blue staining) in MCF7 cells untreated (control) or treated with 7.5 nM bortezomib, 1 μM palbociclib, or a combination of both. Scale bar is 50 μm. Quantification of the β‐galactosidase activity levels is shown in panel (E) ( n = 4). Schematic model of palbociclib action on cell cycle and cell senescence. Data information: In panels (B–D and F), data are presented as means ± SD; each n represents an individual biological replicate. P ‐values were determined by ANOVA and two‐tailed Student's t ‐test with Holm–Sidak post hoc test; ns depicts not significant ( P > 0.05); **: P

    Journal: The EMBO Journal

    Article Title: Thermal proteome profiling of breast cancer cells reveals proteasomal activation by CDK4/6 inhibitor palbociclib

    doi: 10.15252/embj.201798359

    Figure Lengend Snippet: Proteasomal inhibition suppresses palbociclib‐induced senescence phenotype Representative maximum‐intensity projections of MCF7 cells treated with the 1 μM palbociclib and/or 7.5 nM bortezomib. Note that 7.5 nM bortezomib inhibits proteasome only partially. Fixed and permeabilized cells were stained with Alexa Fluor 488‐conjugated Ki67 antibody, Alexa Fluor 647‐conjugated phospho‐Histone H2A.X (γH2AX) (pSer139) antibody, and DAPI. All images were acquired with the same magnification, and scale bar is 20 μm. Flow cytometry‐based quantifications of cell size (B), Ki67 levels (C), and pSer139 γH2AX levels (D) from the samples presented in panel (A) ( n = 4). Senescence‐associated beta‐galactosidase activity (blue staining) in MCF7 cells untreated (control) or treated with 7.5 nM bortezomib, 1 μM palbociclib, or a combination of both. Scale bar is 50 μm. Quantification of the β‐galactosidase activity levels is shown in panel (E) ( n = 4). Schematic model of palbociclib action on cell cycle and cell senescence. Data information: In panels (B–D and F), data are presented as means ± SD; each n represents an individual biological replicate. P ‐values were determined by ANOVA and two‐tailed Student's t ‐test with Holm–Sidak post hoc test; ns depicts not significant ( P > 0.05); **: P

    Article Snippet: Ki67 (D3B5) Alexa Fluor 488 conjugate antibody and phospho‐Histone H2A.X (Ser139; 20E3) Alexa Fluor 647 conjugate antibody were obtained from CST (#11880 and #9720, respectively).

    Techniques: Inhibition, Staining, Flow Cytometry, Cytometry, Activity Assay, Two Tailed Test