ki 67  (Boster Bio)


Bioz Verified Symbol Boster Bio is a verified supplier
Bioz Manufacturer Symbol Boster Bio manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 92

    Structured Review

    Boster Bio ki 67
    miR-184 reduced glioma growth and TNFAIP2 expression in vivo in the mice model. A . shows the T2-weighted MRI imaging of subcutaneous tumor growth at days 25 and 35 in U87-miR-184 and U87-Negative nude mice (red arrows indicate tumors). B .- D . show that miR-184 reduced glioma growth in the subcutaneous glioma nude mice model. E . shows the representative H E staining, which revealed that miR-184 reduced glioma growth in the encephalic glioma nude mice model. F . shows that miR-184 reduced TNFAIP2 and <t>ki-67</t> expression in an in vivo mice model. Data are shown as mean + s.d. (n = 3); *indicates P-value
    Ki 67, supplied by Boster Bio, used in various techniques. Bioz Stars score: 92/100, based on 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ki 67/product/Boster Bio
    Average 92 stars, based on 12 article reviews
    Price from $9.99 to $1999.99
    ki 67 - by Bioz Stars, 2022-11
    92/100 stars

    Images

    1) Product Images from "MicroRNA-184 inhibits cell proliferation and invasion, and specifically targets TNFAIP2 in Glioma"

    Article Title: MicroRNA-184 inhibits cell proliferation and invasion, and specifically targets TNFAIP2 in Glioma

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    doi: 10.1186/s13046-015-0142-9

    miR-184 reduced glioma growth and TNFAIP2 expression in vivo in the mice model. A . shows the T2-weighted MRI imaging of subcutaneous tumor growth at days 25 and 35 in U87-miR-184 and U87-Negative nude mice (red arrows indicate tumors). B .- D . show that miR-184 reduced glioma growth in the subcutaneous glioma nude mice model. E . shows the representative H E staining, which revealed that miR-184 reduced glioma growth in the encephalic glioma nude mice model. F . shows that miR-184 reduced TNFAIP2 and ki-67 expression in an in vivo mice model. Data are shown as mean + s.d. (n = 3); *indicates P-value
    Figure Legend Snippet: miR-184 reduced glioma growth and TNFAIP2 expression in vivo in the mice model. A . shows the T2-weighted MRI imaging of subcutaneous tumor growth at days 25 and 35 in U87-miR-184 and U87-Negative nude mice (red arrows indicate tumors). B .- D . show that miR-184 reduced glioma growth in the subcutaneous glioma nude mice model. E . shows the representative H E staining, which revealed that miR-184 reduced glioma growth in the encephalic glioma nude mice model. F . shows that miR-184 reduced TNFAIP2 and ki-67 expression in an in vivo mice model. Data are shown as mean + s.d. (n = 3); *indicates P-value

    Techniques Used: Expressing, In Vivo, Mouse Assay, Magnetic Resonance Imaging, Imaging, Staining

    Up-miR-184 reduced the invasiveness and growth of glioma cells. A . Wound healing assay shows that the migration of U87 and U251 cells transfected with miR-184 mimics or inhibitor. The overexpression of miR-184 inhibited the wound closure speed of U87 and U251 cells compared with the Negative group or inhibitor group. B . Transwell assay shows the invasion of U87 and U251 cells transfected with miR-184 mimics or inhibitor. which revealed that the numbers of invasive cells were significantly reduced compared with the Negative group or inhibitor group. Each bar represents the mean values from three independent experiments. The invaded cells were counted from 6 random fields. C . shows the cell survival, which was determined by the CCK-8 assay. Cell proliferation was dramatically decreased in U251 and U87 cells after transfection with miR-184. Data are shown as mean + s.d. (n = 3); *indicates P-value
    Figure Legend Snippet: Up-miR-184 reduced the invasiveness and growth of glioma cells. A . Wound healing assay shows that the migration of U87 and U251 cells transfected with miR-184 mimics or inhibitor. The overexpression of miR-184 inhibited the wound closure speed of U87 and U251 cells compared with the Negative group or inhibitor group. B . Transwell assay shows the invasion of U87 and U251 cells transfected with miR-184 mimics or inhibitor. which revealed that the numbers of invasive cells were significantly reduced compared with the Negative group or inhibitor group. Each bar represents the mean values from three independent experiments. The invaded cells were counted from 6 random fields. C . shows the cell survival, which was determined by the CCK-8 assay. Cell proliferation was dramatically decreased in U251 and U87 cells after transfection with miR-184. Data are shown as mean + s.d. (n = 3); *indicates P-value

    Techniques Used: Wound Healing Assay, Migration, Transfection, Over Expression, Transwell Assay, CCK-8 Assay

    2) Product Images from "miR-494-3p Regulates Cellular Proliferation, Invasion, Migration, and Apoptosis by PTEN/AKT Signaling in Human Glioblastoma Cells"

    Article Title: miR-494-3p Regulates Cellular Proliferation, Invasion, Migration, and Apoptosis by PTEN/AKT Signaling in Human Glioblastoma Cells

    Journal: Cellular and Molecular Neurobiology

    doi: 10.1007/s10571-015-0163-0

    miR-494-3P inhibitor reduced cell proliferation and promoted cell apoptosis through PTEN/AKT signaling. a miR-494-3p inhibitor increased the protein expression of PTEN and decreased the protein expression of AKT. b miR-494-3p inhibitor upregulated PTEN mRNA in glioma cells (** p
    Figure Legend Snippet: miR-494-3P inhibitor reduced cell proliferation and promoted cell apoptosis through PTEN/AKT signaling. a miR-494-3p inhibitor increased the protein expression of PTEN and decreased the protein expression of AKT. b miR-494-3p inhibitor upregulated PTEN mRNA in glioma cells (** p

    Techniques Used: Expressing

    miR-494-3p can inhibit the cell proliferation in xenografted tumor model. The expression of Ki-67, PTEN, MMP2, and MMP9 in vivo (×400)
    Figure Legend Snippet: miR-494-3p can inhibit the cell proliferation in xenografted tumor model. The expression of Ki-67, PTEN, MMP2, and MMP9 in vivo (×400)

    Techniques Used: Expressing, In Vivo

    3) Product Images from "miR-494-3p Regulates Cellular Proliferation, Invasion, Migration, and Apoptosis by PTEN/AKT Signaling in Human Glioblastoma Cells"

    Article Title: miR-494-3p Regulates Cellular Proliferation, Invasion, Migration, and Apoptosis by PTEN/AKT Signaling in Human Glioblastoma Cells

    Journal: Cellular and Molecular Neurobiology

    doi: 10.1007/s10571-015-0163-0

    miR-494-3P inhibitor reduced cell proliferation and promoted cell apoptosis through PTEN/AKT signaling. a miR-494-3p inhibitor increased the protein expression of PTEN and decreased the protein expression of AKT. b miR-494-3p inhibitor upregulated PTEN mRNA in glioma cells (** p
    Figure Legend Snippet: miR-494-3P inhibitor reduced cell proliferation and promoted cell apoptosis through PTEN/AKT signaling. a miR-494-3p inhibitor increased the protein expression of PTEN and decreased the protein expression of AKT. b miR-494-3p inhibitor upregulated PTEN mRNA in glioma cells (** p

    Techniques Used: Expressing

    miR-494-3p can inhibit the cell proliferation in xenografted tumor model. The expression of Ki-67, PTEN, MMP2, and MMP9 in vivo (×400)
    Figure Legend Snippet: miR-494-3p can inhibit the cell proliferation in xenografted tumor model. The expression of Ki-67, PTEN, MMP2, and MMP9 in vivo (×400)

    Techniques Used: Expressing, In Vivo

    4) Product Images from "miR-494-3p Regulates Cellular Proliferation, Invasion, Migration, and Apoptosis by PTEN/AKT Signaling in Human Glioblastoma Cells"

    Article Title: miR-494-3p Regulates Cellular Proliferation, Invasion, Migration, and Apoptosis by PTEN/AKT Signaling in Human Glioblastoma Cells

    Journal: Cellular and Molecular Neurobiology

    doi: 10.1007/s10571-015-0163-0

    miR-494-3P inhibitor reduced cell proliferation and promoted cell apoptosis through PTEN/AKT signaling. a miR-494-3p inhibitor increased the protein expression of PTEN and decreased the protein expression of AKT. b miR-494-3p inhibitor upregulated PTEN mRNA in glioma cells (** p
    Figure Legend Snippet: miR-494-3P inhibitor reduced cell proliferation and promoted cell apoptosis through PTEN/AKT signaling. a miR-494-3p inhibitor increased the protein expression of PTEN and decreased the protein expression of AKT. b miR-494-3p inhibitor upregulated PTEN mRNA in glioma cells (** p

    Techniques Used: Expressing

    miR-494-3p can inhibit the cell proliferation in xenografted tumor model. The expression of Ki-67, PTEN, MMP2, and MMP9 in vivo (×400)
    Figure Legend Snippet: miR-494-3p can inhibit the cell proliferation in xenografted tumor model. The expression of Ki-67, PTEN, MMP2, and MMP9 in vivo (×400)

    Techniques Used: Expressing, In Vivo

    5) Product Images from "MicroRNA-16 inhibits glioma cell growth and invasion through suppression of BCL2 and the nuclear factor-κB1/MMP9 signaling pathway"

    Article Title: MicroRNA-16 inhibits glioma cell growth and invasion through suppression of BCL2 and the nuclear factor-κB1/MMP9 signaling pathway

    Journal: Cancer Science

    doi: 10.1111/cas.12351

    miR-16 reduced Ki-67 (a), MMP9 (b), and nuclear factor-κB1 (NF-κB1) (c) expression in an in vivo mouse model using U87 glioma cells. miR-16, microRNA-16.
    Figure Legend Snippet: miR-16 reduced Ki-67 (a), MMP9 (b), and nuclear factor-κB1 (NF-κB1) (c) expression in an in vivo mouse model using U87 glioma cells. miR-16, microRNA-16.

    Techniques Used: Expressing, In Vivo

    6) Product Images from "MicroRNA-16 inhibits glioma cell growth and invasion through suppression of BCL2 and the nuclear factor-κB1/MMP9 signaling pathway"

    Article Title: MicroRNA-16 inhibits glioma cell growth and invasion through suppression of BCL2 and the nuclear factor-κB1/MMP9 signaling pathway

    Journal: Cancer Science

    doi: 10.1111/cas.12351

    miR-16 reduced Ki-67 (a), MMP9 (b), and nuclear factor-κB1 (NF-κB1) (c) expression in an in vivo mouse model using U87 glioma cells. miR-16, microRNA-16.
    Figure Legend Snippet: miR-16 reduced Ki-67 (a), MMP9 (b), and nuclear factor-κB1 (NF-κB1) (c) expression in an in vivo mouse model using U87 glioma cells. miR-16, microRNA-16.

    Techniques Used: Expressing, In Vivo

    7) Product Images from "MicroRNA-16 inhibits glioma cell growth and invasion through suppression of BCL2 and the nuclear factor-κB1/MMP9 signaling pathway"

    Article Title: MicroRNA-16 inhibits glioma cell growth and invasion through suppression of BCL2 and the nuclear factor-κB1/MMP9 signaling pathway

    Journal: Cancer Science

    doi: 10.1111/cas.12351

    miR-16 reduced Ki-67 (a), MMP9 (b), and nuclear factor-κB1 (NF-κB1) (c) expression in an in vivo mouse model using U87 glioma cells. miR-16, microRNA-16.
    Figure Legend Snippet: miR-16 reduced Ki-67 (a), MMP9 (b), and nuclear factor-κB1 (NF-κB1) (c) expression in an in vivo mouse model using U87 glioma cells. miR-16, microRNA-16.

    Techniques Used: Expressing, In Vivo

    8) Product Images from "PlexinA1 expression in gastric carcinoma and its relationship with tumor angiogenesis and proliferation"

    Article Title: PlexinA1 expression in gastric carcinoma and its relationship with tumor angiogenesis and proliferation

    Journal:

    doi: 10.3748/wjg.v13.i48.6558

    Expression of PlexinA1, Ki-67 and VIII factor in gastric carcinoma tissue (S-P × 400). A: PlexinA1; B: Ki-67; C: VIII factor.
    Figure Legend Snippet: Expression of PlexinA1, Ki-67 and VIII factor in gastric carcinoma tissue (S-P × 400). A: PlexinA1; B: Ki-67; C: VIII factor.

    Techniques Used: Expressing

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 94
    Boster Bio anti ki67 antibody sp6
    MSA-2 combined with YM101 therapy improved the activities of tumor-infiltrating immune cells in EMT-6 model. a–d FACS gating strategies for tumor-infiltrating T, NK, DC, and macrophages. e–x In the FACS assays, quantification of CD3 + T, CD8 + T, activated CD8 + T (CD25 + or CD69 + ), effector memory CD8 + T (CD44 + CD62L − ), <t>Ki67</t> + CD8 + T, IFN-γ + CD8 + T, Granzyme-B + CD8 + T, NK, Ki67 + NK, IFN-γ + NK, Granzyme-B + NK, TNF-α + NK, DC, mature DC (CD80 + or CD86 + ), macrophage, M1-like macrophage (MHC-II + CD206 − ), and M2-like macrophage (MHC-II − CD206 + ). Numbers of immune cells per 100 mg EMT-6 tissue were calculated and compared. y The representative immunofluorescent staining images of tumor-infiltrating T cells. Red refers to CD4 + staining, and green refers to CD8 + staining. z Quantification of infiltration depth of T cells. * p
    Anti Ki67 Antibody Sp6, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti ki67 antibody sp6/product/Boster Bio
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti ki67 antibody sp6 - by Bioz Stars, 2022-11
    94/100 stars
      Buy from Supplier

    94
    Boster Bio rabbit anti ki 67 polyclonal antibodies
    Immunohistochemical analysis of Notch1-, <t>Ki-67-,</t> and TUNEL-positive cells in LSCC tissues. a Notch1 was observed in the cell membranes and cytoplasm of cancer cells (×400). b Ki-67 was found in the nuclei of neoplastic cells (×400). c Apoptotic cells were assessed by the TUNEL method (×400)
    Rabbit Anti Ki 67 Polyclonal Antibodies, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti ki 67 polyclonal antibodies/product/Boster Bio
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti ki 67 polyclonal antibodies - by Bioz Stars, 2022-11
    94/100 stars
      Buy from Supplier

    94
    Boster Bio anti ki 67 antibody
    SOAT1 is a downstream target of miR-30a-3p. A RKO and SW480 cells were transfected with miR-30a-3p mimics or inhibitors. SOAT1 expression was scouted by qRT-PCR. B Relative activities of luciferase were measured in HEK293T cells after transfection with SOAT1-Mut or SOAT1-WT and miR-30a-3p mimics or mimic NC. C Overexpression of miR-30a-3p restrained the protein production of SOAT1. Suppression of miR-30a-3p raised the expression of SOAT1 protein. D Knockdown of circLDLR (sh-circLDLR) inhibited the protein expression of SOAT1. Overexpression of circLDLR (circLDLR-OE) increased the protein expression of SOAT1. E Knockdown of miR-30a-3p reversed the sh-circLDLR-induced downregulation of SOAT1 expression in RKO cells. Overexpression of miR-30a-3p reversed the circLDLR-OE-induced upregulation of SOAT1 expression in SW480 cells. GAPDH deeded as a loading control. F EdU analysis of the <t>cell</t> <t>proliferation</t> ability in SW480 and HT29 transfected with miR-30a-3p inhibitors or cotransfected with si-SOAT1 and miR-30a-3p inhibitors. G Cell migration and invasion in SW480 and HT29 transfected with miR-30a-3p inhibitors or cotransfected with si-SOAT1 and miR-30a-3p inhibitors were examined. H The contents of T-CHO and LDL-C in SW480 and HT29 cells transfected with miR-30a-3p inhibitors or cotransfected with si-SOAT1 and miR-30a-3p inhibitors were assessed. I EdU analysis of the cell proliferation ability in SW480 and HT29 transfected with circLDLR-OE or cotransfected with si-SOAT1 and circLDLR-OE. J Cell behaviors of migration and invasion in HT29 and SW480 cells transfected with circLDLR-OE or cotransfected with si-SOAT1 and circLDLR-OE were examined. K The contents of T-CHO and LDL-C in SW480 and HT29 cells transfected with circLDLR-OE or cotransfected with si-SOAT1 and circLDLR-OE were assessed. Data are presented as the mean ± SD of three independent experiments. * P
    Anti Ki 67 Antibody, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti ki 67 antibody/product/Boster Bio
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti ki 67 antibody - by Bioz Stars, 2022-11
    94/100 stars
      Buy from Supplier

    94
    Boster Bio antibodies against ki67
    SOAT1 is a downstream target of miR-30a-3p. A RKO and SW480 cells were transfected with miR-30a-3p mimics or inhibitors. SOAT1 expression was scouted by qRT-PCR. B Relative activities of luciferase were measured in HEK293T cells after transfection with SOAT1-Mut or SOAT1-WT and miR-30a-3p mimics or mimic NC. C Overexpression of miR-30a-3p restrained the protein production of SOAT1. Suppression of miR-30a-3p raised the expression of SOAT1 protein. D Knockdown of circLDLR (sh-circLDLR) inhibited the protein expression of SOAT1. Overexpression of circLDLR (circLDLR-OE) increased the protein expression of SOAT1. E Knockdown of miR-30a-3p reversed the sh-circLDLR-induced downregulation of SOAT1 expression in RKO cells. Overexpression of miR-30a-3p reversed the circLDLR-OE-induced upregulation of SOAT1 expression in SW480 cells. GAPDH deeded as a loading control. F EdU analysis of the <t>cell</t> <t>proliferation</t> ability in SW480 and HT29 transfected with miR-30a-3p inhibitors or cotransfected with si-SOAT1 and miR-30a-3p inhibitors. G Cell migration and invasion in SW480 and HT29 transfected with miR-30a-3p inhibitors or cotransfected with si-SOAT1 and miR-30a-3p inhibitors were examined. H The contents of T-CHO and LDL-C in SW480 and HT29 cells transfected with miR-30a-3p inhibitors or cotransfected with si-SOAT1 and miR-30a-3p inhibitors were assessed. I EdU analysis of the cell proliferation ability in SW480 and HT29 transfected with circLDLR-OE or cotransfected with si-SOAT1 and circLDLR-OE. J Cell behaviors of migration and invasion in HT29 and SW480 cells transfected with circLDLR-OE or cotransfected with si-SOAT1 and circLDLR-OE were examined. K The contents of T-CHO and LDL-C in SW480 and HT29 cells transfected with circLDLR-OE or cotransfected with si-SOAT1 and circLDLR-OE were assessed. Data are presented as the mean ± SD of three independent experiments. * P
    Antibodies Against Ki67, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against ki67/product/Boster Bio
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    antibodies against ki67 - by Bioz Stars, 2022-11
    94/100 stars
      Buy from Supplier

    Image Search Results


    MSA-2 combined with YM101 therapy improved the activities of tumor-infiltrating immune cells in EMT-6 model. a–d FACS gating strategies for tumor-infiltrating T, NK, DC, and macrophages. e–x In the FACS assays, quantification of CD3 + T, CD8 + T, activated CD8 + T (CD25 + or CD69 + ), effector memory CD8 + T (CD44 + CD62L − ), Ki67 + CD8 + T, IFN-γ + CD8 + T, Granzyme-B + CD8 + T, NK, Ki67 + NK, IFN-γ + NK, Granzyme-B + NK, TNF-α + NK, DC, mature DC (CD80 + or CD86 + ), macrophage, M1-like macrophage (MHC-II + CD206 − ), and M2-like macrophage (MHC-II − CD206 + ). Numbers of immune cells per 100 mg EMT-6 tissue were calculated and compared. y The representative immunofluorescent staining images of tumor-infiltrating T cells. Red refers to CD4 + staining, and green refers to CD8 + staining. z Quantification of infiltration depth of T cells. * p

    Journal: Journal of Hematology & Oncology

    Article Title: Combination of oral STING agonist MSA-2 and anti-TGF-β/PD-L1 bispecific antibody YM101: a novel immune cocktail therapy for non-inflamed tumors

    doi: 10.1186/s13045-022-01363-8

    Figure Lengend Snippet: MSA-2 combined with YM101 therapy improved the activities of tumor-infiltrating immune cells in EMT-6 model. a–d FACS gating strategies for tumor-infiltrating T, NK, DC, and macrophages. e–x In the FACS assays, quantification of CD3 + T, CD8 + T, activated CD8 + T (CD25 + or CD69 + ), effector memory CD8 + T (CD44 + CD62L − ), Ki67 + CD8 + T, IFN-γ + CD8 + T, Granzyme-B + CD8 + T, NK, Ki67 + NK, IFN-γ + NK, Granzyme-B + NK, TNF-α + NK, DC, mature DC (CD80 + or CD86 + ), macrophage, M1-like macrophage (MHC-II + CD206 − ), and M2-like macrophage (MHC-II − CD206 + ). Numbers of immune cells per 100 mg EMT-6 tissue were calculated and compared. y The representative immunofluorescent staining images of tumor-infiltrating T cells. Red refers to CD4 + staining, and green refers to CD8 + staining. z Quantification of infiltration depth of T cells. * p

    Article Snippet: The Abs targeting PCNA (BM0104, Boster), Ki67 (ab16667, Abcam), CD8 (ab217344, Abcam), and CD4 (ab183685, Abcam) were used in the assays.

    Techniques: FACS, Staining

    MSA-2 combined with YM101 therapy altered the TME and promoted immunity-associated gene expression in B16 model. a–h Quantification of CD8 + T cell, Ki67 + CD8 + T cell, Perforin + CD8 + T cell, IFN-γ + CD8 + T cell, Granzyme-B + CD8 + T cell, CD69 + CD8 + T cell, NK cell, DC. (i) The heatmap shows the differentially expressed genes among four groups. The levels of immune-killing genes including Prf1 , Tnf , Gzma , and Gzmb were quantitatively analyzed. j–m GO enrichment analysis exploring biological processes significantly enriched in MSA-2 combined with YM101 group. n–s The scores of immune signatures. The heatmaps presenting the scaled expression level of genes constituting immune signatures. * p

    Journal: Journal of Hematology & Oncology

    Article Title: Combination of oral STING agonist MSA-2 and anti-TGF-β/PD-L1 bispecific antibody YM101: a novel immune cocktail therapy for non-inflamed tumors

    doi: 10.1186/s13045-022-01363-8

    Figure Lengend Snippet: MSA-2 combined with YM101 therapy altered the TME and promoted immunity-associated gene expression in B16 model. a–h Quantification of CD8 + T cell, Ki67 + CD8 + T cell, Perforin + CD8 + T cell, IFN-γ + CD8 + T cell, Granzyme-B + CD8 + T cell, CD69 + CD8 + T cell, NK cell, DC. (i) The heatmap shows the differentially expressed genes among four groups. The levels of immune-killing genes including Prf1 , Tnf , Gzma , and Gzmb were quantitatively analyzed. j–m GO enrichment analysis exploring biological processes significantly enriched in MSA-2 combined with YM101 group. n–s The scores of immune signatures. The heatmaps presenting the scaled expression level of genes constituting immune signatures. * p

    Article Snippet: The Abs targeting PCNA (BM0104, Boster), Ki67 (ab16667, Abcam), CD8 (ab217344, Abcam), and CD4 (ab183685, Abcam) were used in the assays.

    Techniques: Expressing

    Immunohistochemical analysis of Notch1-, Ki-67-, and TUNEL-positive cells in LSCC tissues. a Notch1 was observed in the cell membranes and cytoplasm of cancer cells (×400). b Ki-67 was found in the nuclei of neoplastic cells (×400). c Apoptotic cells were assessed by the TUNEL method (×400)

    Journal: World Journal of Surgical Oncology

    Article Title: Effect of Notch1 signaling on cellular proliferation and apoptosis in human laryngeal carcinoma

    doi: 10.1186/s12957-022-02728-6

    Figure Lengend Snippet: Immunohistochemical analysis of Notch1-, Ki-67-, and TUNEL-positive cells in LSCC tissues. a Notch1 was observed in the cell membranes and cytoplasm of cancer cells (×400). b Ki-67 was found in the nuclei of neoplastic cells (×400). c Apoptotic cells were assessed by the TUNEL method (×400)

    Article Snippet: The following primary antibodies were incubated with the tissue sections overnight at 4 °C: rabbit anti-Notch1 monoclonal antibodies (Epitomics, Inc., Burlingame, CA, USA) (1:100 dilution) and rabbit anti-Ki-67 polyclonal antibodies (BA1508, Wuhan Boster, China) (1:800 dilution).

    Techniques: Immunohistochemistry, TUNEL Assay

    SOAT1 is a downstream target of miR-30a-3p. A RKO and SW480 cells were transfected with miR-30a-3p mimics or inhibitors. SOAT1 expression was scouted by qRT-PCR. B Relative activities of luciferase were measured in HEK293T cells after transfection with SOAT1-Mut or SOAT1-WT and miR-30a-3p mimics or mimic NC. C Overexpression of miR-30a-3p restrained the protein production of SOAT1. Suppression of miR-30a-3p raised the expression of SOAT1 protein. D Knockdown of circLDLR (sh-circLDLR) inhibited the protein expression of SOAT1. Overexpression of circLDLR (circLDLR-OE) increased the protein expression of SOAT1. E Knockdown of miR-30a-3p reversed the sh-circLDLR-induced downregulation of SOAT1 expression in RKO cells. Overexpression of miR-30a-3p reversed the circLDLR-OE-induced upregulation of SOAT1 expression in SW480 cells. GAPDH deeded as a loading control. F EdU analysis of the cell proliferation ability in SW480 and HT29 transfected with miR-30a-3p inhibitors or cotransfected with si-SOAT1 and miR-30a-3p inhibitors. G Cell migration and invasion in SW480 and HT29 transfected with miR-30a-3p inhibitors or cotransfected with si-SOAT1 and miR-30a-3p inhibitors were examined. H The contents of T-CHO and LDL-C in SW480 and HT29 cells transfected with miR-30a-3p inhibitors or cotransfected with si-SOAT1 and miR-30a-3p inhibitors were assessed. I EdU analysis of the cell proliferation ability in SW480 and HT29 transfected with circLDLR-OE or cotransfected with si-SOAT1 and circLDLR-OE. J Cell behaviors of migration and invasion in HT29 and SW480 cells transfected with circLDLR-OE or cotransfected with si-SOAT1 and circLDLR-OE were examined. K The contents of T-CHO and LDL-C in SW480 and HT29 cells transfected with circLDLR-OE or cotransfected with si-SOAT1 and circLDLR-OE were assessed. Data are presented as the mean ± SD of three independent experiments. * P

    Journal: Cell Death Discovery

    Article Title: Circular RNA circLDLR facilitates cancer progression by altering the miR-30a-3p/SOAT1 axis in colorectal cancer

    doi: 10.1038/s41420-022-01110-5

    Figure Lengend Snippet: SOAT1 is a downstream target of miR-30a-3p. A RKO and SW480 cells were transfected with miR-30a-3p mimics or inhibitors. SOAT1 expression was scouted by qRT-PCR. B Relative activities of luciferase were measured in HEK293T cells after transfection with SOAT1-Mut or SOAT1-WT and miR-30a-3p mimics or mimic NC. C Overexpression of miR-30a-3p restrained the protein production of SOAT1. Suppression of miR-30a-3p raised the expression of SOAT1 protein. D Knockdown of circLDLR (sh-circLDLR) inhibited the protein expression of SOAT1. Overexpression of circLDLR (circLDLR-OE) increased the protein expression of SOAT1. E Knockdown of miR-30a-3p reversed the sh-circLDLR-induced downregulation of SOAT1 expression in RKO cells. Overexpression of miR-30a-3p reversed the circLDLR-OE-induced upregulation of SOAT1 expression in SW480 cells. GAPDH deeded as a loading control. F EdU analysis of the cell proliferation ability in SW480 and HT29 transfected with miR-30a-3p inhibitors or cotransfected with si-SOAT1 and miR-30a-3p inhibitors. G Cell migration and invasion in SW480 and HT29 transfected with miR-30a-3p inhibitors or cotransfected with si-SOAT1 and miR-30a-3p inhibitors were examined. H The contents of T-CHO and LDL-C in SW480 and HT29 cells transfected with miR-30a-3p inhibitors or cotransfected with si-SOAT1 and miR-30a-3p inhibitors were assessed. I EdU analysis of the cell proliferation ability in SW480 and HT29 transfected with circLDLR-OE or cotransfected with si-SOAT1 and circLDLR-OE. J Cell behaviors of migration and invasion in HT29 and SW480 cells transfected with circLDLR-OE or cotransfected with si-SOAT1 and circLDLR-OE were examined. K The contents of T-CHO and LDL-C in SW480 and HT29 cells transfected with circLDLR-OE or cotransfected with si-SOAT1 and circLDLR-OE were assessed. Data are presented as the mean ± SD of three independent experiments. * P

    Article Snippet: Sections were processed and stained with an anti-Ki-67 antibody (BOSTER, California, USA, #BM4381, 1:50), anti-CD31 antibody (Abcam, Cambridge, MA, USA, #ab32457, 1:1500) or anti-SOAT1 antibody (CST, Beverly, Ma, USA, #35695 S, 1:50).

    Techniques: Transfection, Expressing, Quantitative RT-PCR, Luciferase, Over Expression, Migration

    CircLDLR overexpression facilitates CRC malignant behaviour and increases cholesterol levels in vitro. A The expression of circLDLR in RKO and HCT116 cells transfected with a circLDLR-overexpression vector (circLDLR-OE) or the control vector (Vector) was assessed by qRT-PCR. B Cell proliferation was scouted at the indicated time points by CCK-8 assays evaluating RKO cells and HCT116 cells transfected with circLDLR-OE or Vector. C EdU analysis of the proliferative ability of RKO cells and HCT116 cells transfected with circLDLR-OE or Vector. Representative images are shown. Scale bar, 200 μm. Statistical analysis of the EdU-positive cell percentage in transfected CRC cells is shown in the bar graph. D The cell migration and invasion of CRC cells were examined by Transwell assays after cells were transfected with circLDLR-OE or Vector. Representative images are shown. Scale bar, 200 μm. Statistical analysis of the migrated and invaded cell numbers is shown in the bar graph. E e The production of T-CHO and LDL-C in CRC cells transfected with circLDLR-OE or Vector were appraised. Data are presented as the mean ± SD of three independent experiments. * P

    Journal: Cell Death Discovery

    Article Title: Circular RNA circLDLR facilitates cancer progression by altering the miR-30a-3p/SOAT1 axis in colorectal cancer

    doi: 10.1038/s41420-022-01110-5

    Figure Lengend Snippet: CircLDLR overexpression facilitates CRC malignant behaviour and increases cholesterol levels in vitro. A The expression of circLDLR in RKO and HCT116 cells transfected with a circLDLR-overexpression vector (circLDLR-OE) or the control vector (Vector) was assessed by qRT-PCR. B Cell proliferation was scouted at the indicated time points by CCK-8 assays evaluating RKO cells and HCT116 cells transfected with circLDLR-OE or Vector. C EdU analysis of the proliferative ability of RKO cells and HCT116 cells transfected with circLDLR-OE or Vector. Representative images are shown. Scale bar, 200 μm. Statistical analysis of the EdU-positive cell percentage in transfected CRC cells is shown in the bar graph. D The cell migration and invasion of CRC cells were examined by Transwell assays after cells were transfected with circLDLR-OE or Vector. Representative images are shown. Scale bar, 200 μm. Statistical analysis of the migrated and invaded cell numbers is shown in the bar graph. E e The production of T-CHO and LDL-C in CRC cells transfected with circLDLR-OE or Vector were appraised. Data are presented as the mean ± SD of three independent experiments. * P

    Article Snippet: Sections were processed and stained with an anti-Ki-67 antibody (BOSTER, California, USA, #BM4381, 1:50), anti-CD31 antibody (Abcam, Cambridge, MA, USA, #ab32457, 1:1500) or anti-SOAT1 antibody (CST, Beverly, Ma, USA, #35695 S, 1:50).

    Techniques: Over Expression, In Vitro, Expressing, Transfection, Plasmid Preparation, Quantitative RT-PCR, CCK-8 Assay, Migration

    CircLDLR suppression inhibits CRC malignant behaviour and increases cholesterol levels in vitro. A The circLDLR and mLDLR expression was assessed in RKO and HCT116 cells transfected with five independent siRNAs targeting circLDLR by qRT-PCR. B Cell proliferation was scouted at the indicated time points by CCK-8 assays evaluating HCT116 cells and RKO cells stimulated with si-NC or si-circLDLR. C EdU analysis of the proliferative ability of HCT116 cells and RKO cells treated with si-NC or si-circLDLR. Representative images are shown. Scale bar, 200 μm. Statistical analysis of the EdU-positive cell percentage in transfected GC cells is shown in the bar graph. D The cell migration and invasion of CRC cells were examined by Transwell assays after cells were transfected with si-circLDLR or si-NC. Representative images are shown. Scale bar, 200 μm. Statistical analysis of the migrated and invaded cell numbers is shown in the bar graph. E The production of T-CHO and LDL-C was assessed in CRC cells transfected with si-NC or si-circLDLR. Data are presented as the mean ± SD of three independent experiments. * P

    Journal: Cell Death Discovery

    Article Title: Circular RNA circLDLR facilitates cancer progression by altering the miR-30a-3p/SOAT1 axis in colorectal cancer

    doi: 10.1038/s41420-022-01110-5

    Figure Lengend Snippet: CircLDLR suppression inhibits CRC malignant behaviour and increases cholesterol levels in vitro. A The circLDLR and mLDLR expression was assessed in RKO and HCT116 cells transfected with five independent siRNAs targeting circLDLR by qRT-PCR. B Cell proliferation was scouted at the indicated time points by CCK-8 assays evaluating HCT116 cells and RKO cells stimulated with si-NC or si-circLDLR. C EdU analysis of the proliferative ability of HCT116 cells and RKO cells treated with si-NC or si-circLDLR. Representative images are shown. Scale bar, 200 μm. Statistical analysis of the EdU-positive cell percentage in transfected GC cells is shown in the bar graph. D The cell migration and invasion of CRC cells were examined by Transwell assays after cells were transfected with si-circLDLR or si-NC. Representative images are shown. Scale bar, 200 μm. Statistical analysis of the migrated and invaded cell numbers is shown in the bar graph. E The production of T-CHO and LDL-C was assessed in CRC cells transfected with si-NC or si-circLDLR. Data are presented as the mean ± SD of three independent experiments. * P

    Article Snippet: Sections were processed and stained with an anti-Ki-67 antibody (BOSTER, California, USA, #BM4381, 1:50), anti-CD31 antibody (Abcam, Cambridge, MA, USA, #ab32457, 1:1500) or anti-SOAT1 antibody (CST, Beverly, Ma, USA, #35695 S, 1:50).

    Techniques: In Vitro, Expressing, Transfection, Quantitative RT-PCR, CCK-8 Assay, Migration