Journal: Frontiers in Oncology

Article Title: CXCL1 Regulated by miR-302e Is Involved in Cell Viability and Motility of Colorectal Cancer via Inhibiting JAK-STAT Signaling Pathway

doi: 10.3389/fonc.2020.577229

Figure Lengend Snippet: CXCL1 is highly expressed in CRC. (A) qRT-PCR results showed the expression of CXCL1 in clinical tissue samples (normal: n = 56; tumor: n = 56), (B, C) Expression of CXCL1 mRNA and proteins in normal colorectal mucosa cell line FHC and CRC cell lines SW837, SW480, CaCO2, HT29, as examined by qRT-PCR and Western blot (* p < 0.05).

Article Snippet: Human normal colorectal mucosa cell line FHC (ATCCCRL-1831) and human CRC epithelial cell lines SW837 (ATCCCCL-235), SW480 (ATCCCCL-228), Caco2 (BNCC350772), and HT29 (ATCCHTB-38) were all ordered from American Type Culture Collection (ATCC, Manassas, VA).

Techniques: Quantitative RT-PCR, Expressing, Western Blot

Journal: Frontiers in Oncology

Article Title: CXCL1 Regulated by miR-302e Is Involved in Cell Viability and Motility of Colorectal Cancer via Inhibiting JAK-STAT Signaling Pathway

doi: 10.3389/fonc.2020.577229

Figure Lengend Snippet: Silencing CXCL1 inhibits cell proliferation, migration, invasion and promotes cell apoptosis of CRC. (A) qRT-PCR results showed the relative expression of CXCL1 after sh-CXCL1 and sh-NC were respectively transfected into SW837 and SW480 cells, (B) CCK-8, (C) wound healing assay, (D) Transwell invasion assay (100×), and (E) flow cytometry results showed the effect of silenced CXCL1 on proliferation, migration, invasion, and apoptosis of transfected cells (* p < 0.05).

Article Snippet: Human normal colorectal mucosa cell line FHC (ATCCCRL-1831) and human CRC epithelial cell lines SW837 (ATCCCCL-235), SW480 (ATCCCCL-228), Caco2 (BNCC350772), and HT29 (ATCCHTB-38) were all ordered from American Type Culture Collection (ATCC, Manassas, VA).

Techniques: Migration, Quantitative RT-PCR, Expressing, Transfection, CCK-8 Assay, Wound Healing Assay, Transwell Invasion Assay, Flow Cytometry

Journal: Frontiers in Oncology

Article Title: CXCL1 Regulated by miR-302e Is Involved in Cell Viability and Motility of Colorectal Cancer via Inhibiting JAK-STAT Signaling Pathway

doi: 10.3389/fonc.2020.577229

Figure Lengend Snippet: miR-302e targets CXCL1 in CRC cells. (A) Venn diagram shows the overlapping miRNAs from genes predicted by TargetScan, mirDIP, miRDB, miRSearch, and microRNA databases, (B, C) qRT-PCR results showed the expression level of miR-302e in (B) CRC cell lines SW837, SW480, CaCO2, HT29, and normal colorectal mucosa cell line FHC, as well as in (C) clinical tumor tissue samples and adjacent normal tissue samples (n = 56), (D) Pearson correlation analysis showed that there was a negative correlation between CXCL1 and miR-302e levels, (E) qRT-PCR and Western blot were conducted to show the relative mRNA and protein expression of CXCL1 after miR-302e mimic and mimic NC were transfected into SW480 cells, (F) Dual-luciferase reporter assay was performed to validate the direct targeting relationship between miR-302e and CXCL1 (* p < 0.05).

Article Snippet: Human normal colorectal mucosa cell line FHC (ATCCCRL-1831) and human CRC epithelial cell lines SW837 (ATCCCCL-235), SW480 (ATCCCCL-228), Caco2 (BNCC350772), and HT29 (ATCCHTB-38) were all ordered from American Type Culture Collection (ATCC, Manassas, VA).

Techniques: Quantitative RT-PCR, Expressing, Western Blot, Transfection, Luciferase, Reporter Assay

Journal: iScience

Article Title: CREB3L4 promotes hepatocellular carcinoma progression and decreases sorafenib chemosensitivity by promoting RHEB-mTORC1 signaling pathway

doi: 10.1016/j.isci.2024.108843

Figure Lengend Snippet:

Article Snippet: Phospho-S6 Ribosomal Protein (Ser235/236) , Cell Signaling Technology , Cat#4858S; RRID: AB_2146236.

Techniques: Virus, Recombinant, CCK-8 Assay, Chromatin Immunoprecipitation, Reporter Assay, Expressing, Sequencing, Plasmid Preparation, Software

Journal: iScience

Article Title: Whitening of brown adipose tissue inhibits osteogenic differentiation via secretion of S100A8/A9

doi: 10.1016/j.isci.2024.108857

Figure Lengend Snippet:

Article Snippet: Phospho-S6 (Ser235/236) , Cell Signaling Technology , CAT#2211S; RRID:AB_21.

Techniques: Virus, Negative Control, Recombinant, Staining, Silver Staining, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Real-time Polymerase Chain Reaction, Software

Journal: Frontiers in Pharmacology

Article Title: Dual PI3K/mTOR inhibitor NVP-BEZ235 induces cell cycle arrest via autophagy mediated protein degradation of RPL19 in nephroblastoma cell

doi: 10.3389/fphar.2025.1588722

Figure Lengend Snippet: NVP-BEZ235 inhibited the growth of G401 cells. (A) G401 cells were treated with different concentrations of NVP-BEZ235 (0, 25, 50, 100, 250, and 500 nM) and CCK-8 assay was used to cell viability detection. (B) Treatment of G401 cells with NVP-BEZ235 (100 nM) for different time points followed by detection using CCK-8 assay. (C) The clone formation assay was conducted after G401 cells were treated with NVP-BEZ235 (0, 25, 50, 100, 250 and 500 nM). (D) G401 cells were treated with/without 100 nM NVP-BEZ235, and EdU assay was used to cell proliferation detection. Data are presented as mean ± SD of three independent experiments; * P < 0.05, NC: Negative Control.

Article Snippet: NVP-BEZ235 (Cat. HY-15174, 99.87% purity) was obtained from MedChemExpress (MCE, New Jersey, United States).

Techniques: CCK-8 Assay, Tube Formation Assay, EdU Assay, Negative Control

Journal: Frontiers in Pharmacology

Article Title: Dual PI3K/mTOR inhibitor NVP-BEZ235 induces cell cycle arrest via autophagy mediated protein degradation of RPL19 in nephroblastoma cell

doi: 10.3389/fphar.2025.1588722

Figure Lengend Snippet: NVP-BEZ235 induced cell cycle arrest. (A) G401 cells were treated with NVP-BEZ235 (100 nM), and the levels of Cyclin A1, Cyclin B1, and p21 were quantified by western blot analyses. The blot shown is representative of three independent biological replicates with technical duplicates. (B) The cell cycle phase after NVP-BEZ235 treatment was determined by flow cytometric analysis. Data are presented as mean ± SD of three independent experiments; * P < 0.05, NC: Negative Control.

Article Snippet: NVP-BEZ235 (Cat. HY-15174, 99.87% purity) was obtained from MedChemExpress (MCE, New Jersey, United States).

Techniques: Western Blot, Negative Control

Journal: Frontiers in Pharmacology

Article Title: Dual PI3K/mTOR inhibitor NVP-BEZ235 induces cell cycle arrest via autophagy mediated protein degradation of RPL19 in nephroblastoma cell

doi: 10.3389/fphar.2025.1588722

Figure Lengend Snippet: NVP-BEZ235 downregulated the expression of RPL19 at a protein level. (A) G401 cells were treated with NVP-BEZ235 (0, 25, 50, 100, 250, and 500 nM) and western blot was used to RPL19 expression detection. The blot shown is representative of three independent biological replicates with technical duplicates. (B) The mRNA levels of RPL19 after NVP-BEZ235 treatment were determined by qRT-PCR. Data are presented as mean ± SD of three independent experiments; * P < 0.05, ns: not significant, NC: Negative Control.

Article Snippet: NVP-BEZ235 (Cat. HY-15174, 99.87% purity) was obtained from MedChemExpress (MCE, New Jersey, United States).

Techniques: Expressing, Western Blot, Quantitative RT-PCR, Negative Control

Journal: Frontiers in Pharmacology

Article Title: Dual PI3K/mTOR inhibitor NVP-BEZ235 induces cell cycle arrest via autophagy mediated protein degradation of RPL19 in nephroblastoma cell

doi: 10.3389/fphar.2025.1588722

Figure Lengend Snippet: RPL19 reversed the effect of NVP-BEZ235 on cell cycle. (A) The transfection efficiency of OE-RPL19 in G401 cells was detected by Western blotting. (B) The levels of Cyclin A1, Cyclin B1, and p21 in G401 cells transfected with OE-RPL19 under the treatment of NVP-BEZ235 were detected by western blot. (C) The cell cycle phase in G401 cells transfected with OE-RPL19 after NVP-BEZ235 treatment was determined by flow cytometric analysis. Data are presented as mean ± SD of three independent experiments; * P < 0.05, WT: Wild Type.

Article Snippet: NVP-BEZ235 (Cat. HY-15174, 99.87% purity) was obtained from MedChemExpress (MCE, New Jersey, United States).

Techniques: Transfection, Western Blot

Journal: Frontiers in Pharmacology

Article Title: Dual PI3K/mTOR inhibitor NVP-BEZ235 induces cell cycle arrest via autophagy mediated protein degradation of RPL19 in nephroblastoma cell

doi: 10.3389/fphar.2025.1588722

Figure Lengend Snippet: NVP-BEZ235 induced autophagy in G401 cells. (A) G401 cells were treated with 100 nM NVP-BEZ235 for 0, 4, 8, 12, 18, and 24 h, and western blot was used to LC3 expression detection. (B) G401 cells were treated with 100 nM NVP-BEZ235 and/or 5 µM CQ for 12 h, and the expressions of LC3 and p62 were quantified by western blot. (C) The autophagy flux was observed by transfection with mRFP-GFP-LC3 adenovirus. Data are presented as mean ± SD of three independent experiments; * P < 0.05, NC: Negative Control.

Article Snippet: NVP-BEZ235 (Cat. HY-15174, 99.87% purity) was obtained from MedChemExpress (MCE, New Jersey, United States).

Techniques: Western Blot, Expressing, Transfection, Negative Control

Journal: Frontiers in Pharmacology

Article Title: Dual PI3K/mTOR inhibitor NVP-BEZ235 induces cell cycle arrest via autophagy mediated protein degradation of RPL19 in nephroblastoma cell

doi: 10.3389/fphar.2025.1588722

Figure Lengend Snippet: Inhibition of autophagy attenuated the inhibitory effect of NVP-BEZ235 on RPL19 expression. (A) G401 cells were treated with NVP-BEZ235 and/or 3-MA, and western blot was used to RPL19 expression detection. (B) G401 cells transfected with sh-ATG5 or sh-NC were treated with NVP-BEZ235, and the expression of RPL19 was detected by western blot. (C) G401 cells were treated with NVP-BEZ235 and/or 3-MA, and immunofluorescence analysis was used to RPL19 expression detection. (D) G401 cells were treated with NVP-BEZ235 and/or MG132, and western blot was used to RPL19 expression detection. (E) The interaction of RPL19 and p62 under the treatment of NVP-BEZ235 was detected by co-immunoprecipitation experiment. Data are presented as mean ± SD of three independent experiments; * P < 0.05.

Article Snippet: NVP-BEZ235 (Cat. HY-15174, 99.87% purity) was obtained from MedChemExpress (MCE, New Jersey, United States).

Techniques: Inhibition, Expressing, Western Blot, Transfection, Immunofluorescence, Immunoprecipitation

Journal: Frontiers in Pharmacology

Article Title: Dual PI3K/mTOR inhibitor NVP-BEZ235 induces cell cycle arrest via autophagy mediated protein degradation of RPL19 in nephroblastoma cell

doi: 10.3389/fphar.2025.1588722

Figure Lengend Snippet: NVP-BEZ235 inhibited the growth of nephroblastoma in vivo . (A) Image of the tumor specimen. (B) The tumor volume in each group. (C) The tumor weight in each group. (D) Tumor tissue sections were examined using H&E staining and immunohistochemical staining for Ki67 and RPL19. Data are presented as mean ± SD; * P < 0.05, NC: Negative Control.

Article Snippet: NVP-BEZ235 (Cat. HY-15174, 99.87% purity) was obtained from MedChemExpress (MCE, New Jersey, United States).

Techniques: In Vivo, Staining, Immunohistochemical staining, Negative Control

Journal: iScience

Article Title: EP300 restores the glycolytic activity and anti-tumor function of CD8 + cytotoxic T cells in nasopharyngeal carcinoma

doi: 10.1016/j.isci.2024.108957

Figure Lengend Snippet:

Article Snippet: gentleMACSTM Dissociator , Miltenyi Biotec , Cat#130-093-235.

Techniques: Recombinant, Control, Activation Assay, Reverse Transcription, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Luciferase, Reporter Assay, Sequencing, Software

Journal: Oncotarget

Article Title: HDAC5, a potential therapeutic target and prognostic biomarker, promotes proliferation, invasion and migration in human breast cancer.

doi: 10.18632/oncotarget.9274

Figure Lengend Snippet: Figure 4: LMK-235 inhibits BC cell proliferation and induces apoptosis. A. Structure of the class IIa HDACi LMK-235. B. MDA-MB-231 and Hs-578T cells were treated with DMSO or 50 nM, 500 nM, or 1 μM LMK-235 for 24 hours. The levels of acetyl-histone H3 and total histone H3 were examined by western blot. GAPDH was used as a loading control. C. Hs-578T, MDA-MB-231, MCF-7 and SK-BR-3 cells were treated with LMK-235 (0 to 20 μM) for 24 (left) or 48 (right) hours. Cell proliferation was determined by CCK8 assay. Points indicate the mean of at least three independent experiments. Bars, SD. D. Hs-578T, MDA-MB-231, MCF-7 and SK-BR-3 cells were cultured in 12-well plates and treated with the indicated concentration of LMK-235; survival was measured by clonogenic assay. (Continued )

Article Snippet: Cells were seeded at an approximate concentration and were cultured under standard incubation conditions (37 °C, 95% humidity, 5% CO2) for 24 hours before the following experiments were performed: (1) transfection with sh-HDAC5 (Origene) or a scrambled control shRNA sequence, (2) treatment with LMK-235 (Selleck Chemicals) or DMSO (vehicle control), (3) treatment with bortezomib (Selleck Chemicals) or DMSO, and (4) treatment with both LMK-235 and bortezomib or DMSO.

Techniques: Western Blot, Control, CCK-8 Assay, Cell Culture, Concentration Assay, Clonogenic Assay

Journal: Oncotarget

Article Title: HDAC5, a potential therapeutic target and prognostic biomarker, promotes proliferation, invasion and migration in human breast cancer.

doi: 10.18632/oncotarget.9274

Figure Lengend Snippet: Figure 5: LMK-235 synergizes with bortezomib in BC cells. A. MDA-MB-231 and Hs-578T cells were treated 50 nM bortezomib or DMSO for 48 hours after transfection with sh-HDAC5#B and sh-HDAC5#D. Cell growth was evaluated by CCK8 assay. Columns, mean ±SD of three independent experiments. **p<0.05 compared with non-treated negative control cells. *p<0.05 compared with treated knockdown cells. B. MDA-MB-231 and Hs-578T cells were treated with various combinations of LMK-235 and bortezomib for 48 hours. Cell viability was determined by CCK8 assay. Points indicate the mean of three independent experiments. C. Synergism of proliferation inhibition of MDA-MB-231 and Hs-578T cells was analyzed by isobologram analysis. D, E. and G. MDA-MB-231 and Hs-578T cells were treated with 1.25 µM LMK-235 and/or 50 nM bortezomib or with 1.25 µM LMK-235 and/or 25 nM bortezomib for 24 hours. (Continued )

Article Snippet: Cells were seeded at an approximate concentration and were cultured under standard incubation conditions (37 °C, 95% humidity, 5% CO2) for 24 hours before the following experiments were performed: (1) transfection with sh-HDAC5 (Origene) or a scrambled control shRNA sequence, (2) treatment with LMK-235 (Selleck Chemicals) or DMSO (vehicle control), (3) treatment with bortezomib (Selleck Chemicals) or DMSO, and (4) treatment with both LMK-235 and bortezomib or DMSO.

Techniques: Transfection, CCK-8 Assay, Negative Control, Knockdown, Inhibition

Journal: Oncotarget

Article Title: HDAC5, a potential therapeutic target and prognostic biomarker, promotes proliferation, invasion and migration in human breast cancer.

doi: 10.18632/oncotarget.9274

Figure Lengend Snippet: Figure 5: (Continued ) LMK-235 synergizes with bortezomib in BC cells. D. Apoptosis was assessed by annexin V/PE-7AAD staining and flow cytometry; representative results are shown. Columns represent the mean ±SD of at least three independent experiments. *p<0.05 compared with the DMSO group; **p<0.05 compared with the equivalent doses in the LMK-235- or bortezomib-treated groups. E. Cell lysates were immunoblotted with anti-caspase 8, anti-caspase 9, anti-Bim and anti-PARP. GAPDH was used as a loading control. F. MDA-MB-231 and Hs-578T cells were plated in Matrigel invasion chambers and treated with 200 nM LMK-235 and/or 5 nM bortezomib for 24 hours. Three separate experiments were conducted, and representative results are shown. Magnification, ×100. Columns indicate the average number of invading cells from 5 random microscopic fields. *p<0.05 compared with the DMSO group; **p<0.05 compared with the equivalent doses in the LMK-235- or bortezomib-treated groups. G. Cell lysates were immunoblotted with anti-MMP2, anti-MMP7 and anti-MMP9 antibodies. GAPDH was used as a loading control.

Article Snippet: Cells were seeded at an approximate concentration and were cultured under standard incubation conditions (37 °C, 95% humidity, 5% CO2) for 24 hours before the following experiments were performed: (1) transfection with sh-HDAC5 (Origene) or a scrambled control shRNA sequence, (2) treatment with LMK-235 (Selleck Chemicals) or DMSO (vehicle control), (3) treatment with bortezomib (Selleck Chemicals) or DMSO, and (4) treatment with both LMK-235 and bortezomib or DMSO.

Techniques: Staining, Flow Cytometry, Control

Journal: iScience

Article Title: Activated PRDM1-CREBBP contributes to preeclampsia by regulating apoptosis and invasion of the human trophoblast cells

doi: 10.1016/j.isci.2024.111484

Figure Lengend Snippet: PRDM1 expression in placentas from EOPE and healthy pregnant women (A) A total of 13 PRDM members were identified via high-throughput transcriptome sequencing. Graph showing gene expression between groups. p value < 0.05 and |log 2 FC| > 1 were considered significant. (B) The mRNA expression of PRDM1 in placentas was detected by real-time PCR (EOPE; n = 4; NP; n = 6). (C) Representative western blots of PRDM1 from four patients with EOPE and the healthy controls in placentas (left); the quantified relative gene expression levels of PRDM1 (right) ( n = 4). (D) The localization and expression of PRDM1 in villous were analyzed by immunohistology. Photographs were obtained at 200× and 400× magnification. Scale bar: 100 and 50 μm. (E) Double immunofluorescence staining of term human placenta tissue indicated nuclear expression and colocalization of PRDM1 to the CK7, marker for trophoblast cells. Nuclei were counterstained with DAPI. Scale bar: 50 μm. (F) The localization and expression of HLA-G (marker for EVTs) and PRDM1 basal plate were analyzed by immunohistology. Photographs were obtained at 200× and 400× magnification. Scale bar: 100 and 50 μm. Data are presented as mean ± SD. ∗∗, p < 0.01, EOPE vs. NP. CV, chorionic villi; BP, basal plate.

Article Snippet: The primary antibodies including: PRDM1 (1:1000; Novus Biologicals, cat# NB600-235, China), CREBBP (1:500; Affinity, cat# AF0861, China), MMP2 (1:500; Proteintech, cat# 10373-2-AP, China), and MMP9 (1:1000; Proteintech, cat# 10375-2-AP, China).

Techniques: Expressing, High Throughput Screening Assay, Sequencing, Gene Expression, Real-time Polymerase Chain Reaction, Western Blot, Double Immunofluorescence Staining, Marker

Journal: iScience

Article Title: Activated PRDM1-CREBBP contributes to preeclampsia by regulating apoptosis and invasion of the human trophoblast cells

doi: 10.1016/j.isci.2024.111484

Figure Lengend Snippet: Upregulation of PRDM1 in the placentas of L-NAME-treated Sprague-Dawley rats (A) Relative protein and mRNA expression of PRDM1 in placentas were detected by western blot analysis and real-time PCR ( n = 6). (B) Representative images of immunohistochemical staining for PRDM1 in placenta tissues. Photographs were obtained at 200× and 400× magnification. Scale bar: 100 and 50 μm. (C) Double immunofluorescence staining of rat placental tissue indicated nuclear expression and colocalization of PRDM1 to the CK7 and HLA-G. Nuclei were counterstained with DAPI. Scale bar: 50 μm. Data are presented as mean ± SD. ∗∗ p < 0.01, L-NAME vs. N.S.

Article Snippet: The primary antibodies including: PRDM1 (1:1000; Novus Biologicals, cat# NB600-235, China), CREBBP (1:500; Affinity, cat# AF0861, China), MMP2 (1:500; Proteintech, cat# 10373-2-AP, China), and MMP9 (1:1000; Proteintech, cat# 10375-2-AP, China).

Techniques: Expressing, Western Blot, Real-time Polymerase Chain Reaction, Immunohistochemical staining, Staining, Double Immunofluorescence Staining

Journal: iScience

Article Title: Activated PRDM1-CREBBP contributes to preeclampsia by regulating apoptosis and invasion of the human trophoblast cells

doi: 10.1016/j.isci.2024.111484

Figure Lengend Snippet: Effect of PRDM1 silencing on growth and invasion of isolated primary trophoblasts (A) Relative protein and mRNA expression of PRDM1 in isolated primary trophoblasts ( n = 3). (B) CCK-8 assay was implemented to detect cell viability ( n = 3). (C) Cell apoptosis was measured using Annexin V-FITC assays and flow cytometry ( n = 3). (D) Transwell detection revealed the invasion and migration capability of isolated primary trophoblasts ( n = 3). Scale bar: 100 μm. Data are presented as mean ± SD. ∗∗ p < 0.01, H/R vs. Con; && p < 0.01, H/R + shPRDM1 vs. H/R + shNEG.

Article Snippet: The primary antibodies including: PRDM1 (1:1000; Novus Biologicals, cat# NB600-235, China), CREBBP (1:500; Affinity, cat# AF0861, China), MMP2 (1:500; Proteintech, cat# 10373-2-AP, China), and MMP9 (1:1000; Proteintech, cat# 10375-2-AP, China).

Techniques: Isolation, Expressing, CCK-8 Assay, Flow Cytometry, Migration

Journal: iScience

Article Title: Activated PRDM1-CREBBP contributes to preeclampsia by regulating apoptosis and invasion of the human trophoblast cells

doi: 10.1016/j.isci.2024.111484

Figure Lengend Snippet: H/R promotes the binding of PRDM1 to CREBBP’s promoter (A) The correlation between PRDM1 and CREBBP expression was detected by Pearson’s correlation. (B) HEK293 cells were co-transfected with indicated plasmids. Luciferase activity was determined. (C) ChIP assays were carried out, and the CREBBP promoter regions containing PRDM1-binding sites 1, 2, and 3 were amplified by PCR. (D) Oligonucleotide pull-down assay was performed by using biotinylated double-stranded oligonucleotide probes. DNA proteins were analyzed by western blot with an anti-PRDM1 antibody. (E) The mRNA expression of CREBBP in trophoblast cells was detected by real-time PCR ( n = 3). Data are presented as mean ± SD. ∗∗ p < 0.01, pcDNA-empty vs. pcDNA-PRDM1; && p < 0.01, H/R + shPRDM1 vs. H/R + shNEG.

Article Snippet: The primary antibodies including: PRDM1 (1:1000; Novus Biologicals, cat# NB600-235, China), CREBBP (1:500; Affinity, cat# AF0861, China), MMP2 (1:500; Proteintech, cat# 10373-2-AP, China), and MMP9 (1:1000; Proteintech, cat# 10375-2-AP, China).

Techniques: Binding Assay, Expressing, Transfection, Luciferase, Activity Assay, Amplification, Pull Down Assay, Western Blot, Real-time Polymerase Chain Reaction

Journal: iScience

Article Title: Activated PRDM1-CREBBP contributes to preeclampsia by regulating apoptosis and invasion of the human trophoblast cells

doi: 10.1016/j.isci.2024.111484

Figure Lengend Snippet: Knockdown of CREBBP abrogated PRDM1 overexpression-mediated alterations of trophoblasts We silenced CREBBP expressing in PRDM1-overexpressed trophoblast cells. (A–C) CCK-8 assay ( n = 3), Annexin V-FITC assays ( n = 3), and Transwell detection in HTR-8/SVneo cells ( n = 3). Scale bar: 100 μm. Data are presented as mean ± SD. ∗∗ p < 0.01, oePRDM1 + shCREBBP vs. oePRDM1 + shNEG.

Article Snippet: The primary antibodies including: PRDM1 (1:1000; Novus Biologicals, cat# NB600-235, China), CREBBP (1:500; Affinity, cat# AF0861, China), MMP2 (1:500; Proteintech, cat# 10373-2-AP, China), and MMP9 (1:1000; Proteintech, cat# 10375-2-AP, China).

Techniques: Knockdown, Over Expression, Expressing, CCK-8 Assay

Journal: iScience

Article Title: Activated PRDM1-CREBBP contributes to preeclampsia by regulating apoptosis and invasion of the human trophoblast cells

doi: 10.1016/j.isci.2024.111484

Figure Lengend Snippet:

Article Snippet: The primary antibodies including: PRDM1 (1:1000; Novus Biologicals, cat# NB600-235, China), CREBBP (1:500; Affinity, cat# AF0861, China), MMP2 (1:500; Proteintech, cat# 10373-2-AP, China), and MMP9 (1:1000; Proteintech, cat# 10375-2-AP, China).

Techniques: Recombinant, In Situ, ATP Assay, Luciferase, Isolation, Software