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MedChemExpress hy 151427
Hy 151427, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/hy+151427/TGF%CE%B21-IN-1/pm40961618-88-14-15
Average 94 stars, based on 11 article reviews

hy 151427 - by Bioz Stars, 2026-09

94/100 stars

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Article Title: Heparanase and MMP-9 synergistically induce endothelial-mesenchymal transition in portal vein microvessels to promote hepatocellular carcinoma metastasis.
Article Snippet: Background: Both heparanase (HPSE) and matrix metalloproteinase-9 (MMP-9) can promote metastasis of hepatocellular carcinoma (HCC), but it is not clear whether they co-induce endothelial-mesenchymal transition (EndoMT) in portal vein endothelial cells (PVECs) to facilitate HCC metastasis.. This study aimed to investigate the combined effect of HPSE and MMP-9 on EndoMT in PVECs and subsequent intrahepatic metastasis of HCC and to explore the underlying mechanism.. Methods: This study employed gene knockdown, gene overexpression and inhibitor strategies to manipulate HPSE/MMP-9 expression or activity within HCC cells, which were non-contact co-cultured with human umbilical vein endothelial cells (HUVECs).

Concentration Assay:

Article Title: S100A2 activation promotes interstitial fibrosis in kidneys by FoxO1-mediated epithelial-mesenchymal transition.
Article Snippet: The cells were also exposed to 200 ng/ml of recombinant S100A2 protein (MCE, USA) or 50 μM SRT1460 (MCE) for 24 hours. .. In this study, HK2 cells were treated with TGFβ1-IN-1 (HY-151427, MCE), a specific TGFβ1 inhibitor, at a concentration of 20 μM for 24 hours to evaluate its efficacy in blocking the effects of TGF-β1 on S100A2 expression. ..

Article Title: S100A2 activation promotes interstitial fibrosis in kidneys by FoxO1-mediated epithelial-mesenchymal transition
Article Snippet: The cells were also exposed to 200 ng/ml of recombinant S100A2 protein (MCE, USA) or 50 μM SRT1460 (MCE) for 24 hours. .. In this study, HK2 cells were treated with TGFβ1-IN-1 (HY-151427, MCE), a specific TGF-β1 inhibitor, at a concentration of 20 μM for 24 hours to evaluate its efficacy in blocking the effects of TGF-β1 on S100A2 expression. ..

Blocking Assay:

Expressing:

Image Search Results

Shh expression is upregulated in the MCAO/R-induced fibrosis mouse model in vivo and TGF-β1-induced fibrosis model in vitro . (A) Timeline of in vivo experiments. Created with BioRender.com. (B) Schematic representation of rat brain coronal section; tested areas are demarcated by squares. Created with BioRender.com. (C, D) Shh concentration in serum and cerebral spinal fluid (CSF) in rats of the MCAO/R group at 7 days after injury (MCAO/R 7 d) and Sham group by ELISA ( n = 6). (E) Representative immunofluorescence images of Fn (green) and DAPI (blue) in rats in the Sham and MCAO/R 7 d groups. Scale bars: 100 µm. (F, G) Western blot of Shh protein expression and quantification data in the Sham and MCAO/R 7 d groups ( n = 3). (H, I) Representative immunofluorescence images of α-SMA/Shh- and FN/Shh-positive cells in rats in the Sham and MCAO/R 7 d groups. Scale bars: 20 µm. (J) Timeline of in vitro experiments. Created with BioRender.com. (K) ELISA evaluation of Shh concentration in the conditioned medium of the TGF-β1 group after 3 days of treatment and Con groups ( n = 6). (L, M) Western blot of Shh protein expression and quantification data in the TGF-β1 and Con groups ( n = 3). Data are expressed as mean ± SD. * P < 0.05, vs . Sham or Con group (two-tailed Student’s t -test). (N, O) Representative immunofluorescence images of α-SMA (red)/Shh (green)- and FN (red)/Shh (green)-positive cells in the TGF-β1 and Con groups. Scale bars: 20 µm. Con: Control; DAPI: 4′,6-diamidino-2-phenylindole; ELISA: enzyme-linked immunosorbent assay; Fn: fibronectin; MCAO/R: middle cerebral artery occlusion/reperfusion; Shh: Sonic hedgehog; TGF-β1: transforming growth factor-beta 1; WB: western blot; α-SMA: alpha-smooth muscle actin.

Journal: Neural Regeneration Research

Article Title: Fibrotic scar formation after cerebral ischemic stroke: Targeting the Sonic hedgehog signaling pathway for scar reduction

doi: 10.4103/NRR.NRR-D-24-00999

Figure Lengend Snippet: Shh expression is upregulated in the MCAO/R-induced fibrosis mouse model in vivo and TGF-β1-induced fibrosis model in vitro . (A) Timeline of in vivo experiments. Created with BioRender.com. (B) Schematic representation of rat brain coronal section; tested areas are demarcated by squares. Created with BioRender.com. (C, D) Shh concentration in serum and cerebral spinal fluid (CSF) in rats of the MCAO/R group at 7 days after injury (MCAO/R 7 d) and Sham group by ELISA ( n = 6). (E) Representative immunofluorescence images of Fn (green) and DAPI (blue) in rats in the Sham and MCAO/R 7 d groups. Scale bars: 100 µm. (F, G) Western blot of Shh protein expression and quantification data in the Sham and MCAO/R 7 d groups ( n = 3). (H, I) Representative immunofluorescence images of α-SMA/Shh- and FN/Shh-positive cells in rats in the Sham and MCAO/R 7 d groups. Scale bars: 20 µm. (J) Timeline of in vitro experiments. Created with BioRender.com. (K) ELISA evaluation of Shh concentration in the conditioned medium of the TGF-β1 group after 3 days of treatment and Con groups ( n = 6). (L, M) Western blot of Shh protein expression and quantification data in the TGF-β1 and Con groups ( n = 3). Data are expressed as mean ± SD. * P < 0.05, vs . Sham or Con group (two-tailed Student’s t -test). (N, O) Representative immunofluorescence images of α-SMA (red)/Shh (green)- and FN (red)/Shh (green)-positive cells in the TGF-β1 and Con groups. Scale bars: 20 µm. Con: Control; DAPI: 4′,6-diamidino-2-phenylindole; ELISA: enzyme-linked immunosorbent assay; Fn: fibronectin; MCAO/R: middle cerebral artery occlusion/reperfusion; Shh: Sonic hedgehog; TGF-β1: transforming growth factor-beta 1; WB: western blot; α-SMA: alpha-smooth muscle actin.

Article Snippet: In in vitro experiments, cells were pre-treated with TGF-β1 (10 ng/mL, MCE, HEK293) for 3 days.

Techniques: Expressing, In Vivo, In Vitro, Concentration Assay, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Western Blot, Two Tailed Test, Control

Shh signaling regulates the expression of MFN2 in vitro and in vivo . (A, B) Western blot analysis of MFN2 protein expression and quantification data in the Sham and MCAO/R 7 d groups ( n = 3). (C) Representative immunofluorescence images of α-SMA (red)/MFN2 (green)- and Fn (red)/MFN2 (green)-positive cells in the Sham and MCAO/R 7 d groups. Scale bars: 20 µm. (D, E) Western blot analysis of MFN2 protein expression and quantification data in the Sham, MCAO/R, MCAO/R + rAd-Shh and MCAO/R + rAd-HK groups ( n = 3). (F) Representative immunofluorescence images of α-SMA (red)/MFN2 (green)- and Fn (red)/MFN2 (green)-positive cells in the Sham, MCAO/R, MCAO/R + rAd-Shh and MCAO/R + rAd-HK groups. (G, H) Western blot analysis of MFN2 protein expression and quantification data in the Con and TGF-β1 groups ( n = 3). (I) Representative immunofluorescence images of α-SMA (red)/MFN2 (green)- and Fn (red)/MFN2 (green)-positive cells in the Con and TGF-β1 groups. Scale bars: 20 µm. (J, K) Western blot analysis of MFN2 protein expression and quantification data in the Con, rAd-HK and rAd-Shh groups ( n = 3). (L, M) Western blot analysis of MFN2 protein expression and quantification data in the Con, SAG and DMSO groups ( n = 3). (N) Representative immunofluorescence images of Fn (red)/MFN2 (green)-positive cells in the Con, rAd-HK and rAd-Shh groups and the Con, SAG and DMSO groups. Scale bars: 20 µm. Data are expressed as mean ± SD. * P < 0.05, vs . Sham or Con group; # P < 0.05, vs. MCAO/R group; & P < 0.05, vs . MCAO/R + rAd-Shh group (B, H: two-tailed Student’s t -test; E, K M: one-way analysis of variance followed by Tukey’s post hoc test). Con: Control; DAPI: 4′,6-diamidino-2-phenylindole; DMSO: dimethyl sulfoxide; Fn: fibronectin; MCAO/R: middle cerebral artery occlusion/reperfusion; MFN2: mitofusin 2; rAd-HK: adenoviral control vector; rAd-Shh: recombinant adenovirus-sonic hedgehog; SAG: Smoothened agonist; TGF-β1: transforming growth factor-beta 1; α-SMA: alpha-smooth muscle actin.

Journal: Neural Regeneration Research

Article Title: Fibrotic scar formation after cerebral ischemic stroke: Targeting the Sonic hedgehog signaling pathway for scar reduction

doi: 10.4103/NRR.NRR-D-24-00999

Figure Lengend Snippet: Shh signaling regulates the expression of MFN2 in vitro and in vivo . (A, B) Western blot analysis of MFN2 protein expression and quantification data in the Sham and MCAO/R 7 d groups ( n = 3). (C) Representative immunofluorescence images of α-SMA (red)/MFN2 (green)- and Fn (red)/MFN2 (green)-positive cells in the Sham and MCAO/R 7 d groups. Scale bars: 20 µm. (D, E) Western blot analysis of MFN2 protein expression and quantification data in the Sham, MCAO/R, MCAO/R + rAd-Shh and MCAO/R + rAd-HK groups ( n = 3). (F) Representative immunofluorescence images of α-SMA (red)/MFN2 (green)- and Fn (red)/MFN2 (green)-positive cells in the Sham, MCAO/R, MCAO/R + rAd-Shh and MCAO/R + rAd-HK groups. (G, H) Western blot analysis of MFN2 protein expression and quantification data in the Con and TGF-β1 groups ( n = 3). (I) Representative immunofluorescence images of α-SMA (red)/MFN2 (green)- and Fn (red)/MFN2 (green)-positive cells in the Con and TGF-β1 groups. Scale bars: 20 µm. (J, K) Western blot analysis of MFN2 protein expression and quantification data in the Con, rAd-HK and rAd-Shh groups ( n = 3). (L, M) Western blot analysis of MFN2 protein expression and quantification data in the Con, SAG and DMSO groups ( n = 3). (N) Representative immunofluorescence images of Fn (red)/MFN2 (green)-positive cells in the Con, rAd-HK and rAd-Shh groups and the Con, SAG and DMSO groups. Scale bars: 20 µm. Data are expressed as mean ± SD. * P < 0.05, vs . Sham or Con group; # P < 0.05, vs. MCAO/R group; & P < 0.05, vs . MCAO/R + rAd-Shh group (B, H: two-tailed Student’s t -test; E, K M: one-way analysis of variance followed by Tukey’s post hoc test). Con: Control; DAPI: 4′,6-diamidino-2-phenylindole; DMSO: dimethyl sulfoxide; Fn: fibronectin; MCAO/R: middle cerebral artery occlusion/reperfusion; MFN2: mitofusin 2; rAd-HK: adenoviral control vector; rAd-Shh: recombinant adenovirus-sonic hedgehog; SAG: Smoothened agonist; TGF-β1: transforming growth factor-beta 1; α-SMA: alpha-smooth muscle actin.

Article Snippet: In in vitro experiments, cells were pre-treated with TGF-β1 (10 ng/mL, MCE, HEK293) for 3 days.

Techniques: Expressing, In Vitro, In Vivo, Western Blot, Immunofluorescence, Two Tailed Test, Control, Plasmid Preparation, Recombinant

Bioinformatics Analysis Atlas. A : Sample correction box plot; B : Sample difference PCA plot; C : Differential gene volcano plot; D : GO enrichment analysis bar chart; E : KEGG enrichment analysis bubble plot; F : KEGG enrichment analysis distance plot; G : Correlation scatter plot of NFIC and PTEN; H : Correlation scatter plot of NFIC and TGFβ1; I : Correlation scatter plot of TGFβ1 and TBX3; J : Correlation scatter plot of TGFβ1 and Egr1; K : Correlation scatter plot of EZH2 and TGFβ1; L : Correlation scatter plot of TGFβ1 and TBX2; M : Correlation scatter plot of TBX3 and TBX2; N : Validation Heatmap of the TCGA-OV Cohort.

Journal: Scientific Reports

Article Title: NFIC suppressed the epithelial ovarian cancer via modulating the balance of PTEN/TGFβ1/EGR1/BRD4 and SP1/EZH2 induced Inhibition of TBX2/MMPs signaling

doi: 10.1038/s41598-025-09653-0

Figure Lengend Snippet: Bioinformatics Analysis Atlas. A : Sample correction box plot; B : Sample difference PCA plot; C : Differential gene volcano plot; D : GO enrichment analysis bar chart; E : KEGG enrichment analysis bubble plot; F : KEGG enrichment analysis distance plot; G : Correlation scatter plot of NFIC and PTEN; H : Correlation scatter plot of NFIC and TGFβ1; I : Correlation scatter plot of TGFβ1 and TBX3; J : Correlation scatter plot of TGFβ1 and Egr1; K : Correlation scatter plot of EZH2 and TGFβ1; L : Correlation scatter plot of TGFβ1 and TBX2; M : Correlation scatter plot of TBX3 and TBX2; N : Validation Heatmap of the TCGA-OV Cohort.

Article Snippet: The PTEN inhibitor SF1670 was purchased from SELECK, and the TGFβ1 inhibitor TGFβ1-IN-1 from MCE.

Techniques: Biomarker Discovery

NFIC inhibits the development of epithelial ovarian cancer, while TBX2 promotes the progression of epithelial ovarian cancer. A : Subcutaneous tumor transplantation experiment results in nude mice and statistical graphs of tumor volume and weight for the NC group, NFIC-OE group, NFIC-OE + TBX2-OE group, NFIC-KD group, NFIC-KD + PTEN-OE group, and NFIC-KD + PTEN-OE + TGFβ1-KD group; B : Subcutaneous tumor transplantation experiment results in nude mice and statistical graphs of tumor volume and weight for the NC group, and TBX2-OE group; C : Immunohistochemical staining results for the NC group, NFIC-OE group, NFIC-OE + TBX2-OE group, NFIC-KD group, NFIC-KD + PTEN-OE group, and NFIC-KD + PTEN-OE + TGFβ1-KD group, along with statistical graphs showing the expression levels of NFIC and TBX2. Data are expressed as mean ± standard deviation. N = 6; ** P <0.01; ns P >0.05.

Journal: Scientific Reports

Article Title: NFIC suppressed the epithelial ovarian cancer via modulating the balance of PTEN/TGFβ1/EGR1/BRD4 and SP1/EZH2 induced Inhibition of TBX2/MMPs signaling

doi: 10.1038/s41598-025-09653-0

Figure Lengend Snippet: NFIC inhibits the development of epithelial ovarian cancer, while TBX2 promotes the progression of epithelial ovarian cancer. A : Subcutaneous tumor transplantation experiment results in nude mice and statistical graphs of tumor volume and weight for the NC group, NFIC-OE group, NFIC-OE + TBX2-OE group, NFIC-KD group, NFIC-KD + PTEN-OE group, and NFIC-KD + PTEN-OE + TGFβ1-KD group; B : Subcutaneous tumor transplantation experiment results in nude mice and statistical graphs of tumor volume and weight for the NC group, and TBX2-OE group; C : Immunohistochemical staining results for the NC group, NFIC-OE group, NFIC-OE + TBX2-OE group, NFIC-KD group, NFIC-KD + PTEN-OE group, and NFIC-KD + PTEN-OE + TGFβ1-KD group, along with statistical graphs showing the expression levels of NFIC and TBX2. Data are expressed as mean ± standard deviation. N = 6; ** P <0.01; ns P >0.05.

Article Snippet: The PTEN inhibitor SF1670 was purchased from SELECK, and the TGFβ1 inhibitor TGFβ1-IN-1 from MCE.

Techniques: Transplantation Assay, Immunohistochemical staining, Staining, Expressing, Standard Deviation

NFIC specifically targets PTEN, TBX2, and TGFβ1. A : Western blot analysis of protein bands for NFIC, PTEN, TBX2, and EZH2 in the NC group and NFIC-KD group, along with statistical graphs of relative protein expression levels; B : Western blot analysis of NFIC protein bands in KGN and SKOV3 cells, along with statistical graphs of relative protein expression levels; GAPDH as control protein; C : Co-Immunoprecipitation experiment results diagram. Data are expressed as mean ± standard deviation. N = 3; ** P <0.01.

Journal: Scientific Reports

Article Title: NFIC suppressed the epithelial ovarian cancer via modulating the balance of PTEN/TGFβ1/EGR1/BRD4 and SP1/EZH2 induced Inhibition of TBX2/MMPs signaling

doi: 10.1038/s41598-025-09653-0

Figure Lengend Snippet: NFIC specifically targets PTEN, TBX2, and TGFβ1. A : Western blot analysis of protein bands for NFIC, PTEN, TBX2, and EZH2 in the NC group and NFIC-KD group, along with statistical graphs of relative protein expression levels; B : Western blot analysis of NFIC protein bands in KGN and SKOV3 cells, along with statistical graphs of relative protein expression levels; GAPDH as control protein; C : Co-Immunoprecipitation experiment results diagram. Data are expressed as mean ± standard deviation. N = 3; ** P <0.01.

Article Snippet: The PTEN inhibitor SF1670 was purchased from SELECK, and the TGFβ1 inhibitor TGFβ1-IN-1 from MCE.

Techniques: Western Blot, Expressing, Control, Immunoprecipitation, Standard Deviation

NFIC acts on epithelial ovarian cancer through PTEN and TGFβ1. A : Western blot protein banding plots of NFIC, TBX2, PTEN, nucleus SP1, nucleus EZH2 and nucleus BRD4 as well as statistical plots of relative protein expression in NC group, NFIC-OE group, NFIC-OE + TBX2-OE group, NFIC-OE + SF1670 group and NFIC-OE + SF1670 + TGFβ1-IN-1 group; B : Western blot protein banding plots of TGFβ1, TBX3, TBX2 as well as statistical plots of relative protein expression in NC group, NFIC-OE group, NFIC-OE + TBX2-OE group, NFIC-OE + SF1670 group and NFIC-OE + SF1670 + TGFβ1-IN-1 group. GAPDH as control protein; Data are expressed as mean ± standard deviation. N = 3; ** P <0.01; * P <0.05; ns P >0.05.

Journal: Scientific Reports

Article Title: NFIC suppressed the epithelial ovarian cancer via modulating the balance of PTEN/TGFβ1/EGR1/BRD4 and SP1/EZH2 induced Inhibition of TBX2/MMPs signaling

doi: 10.1038/s41598-025-09653-0

Figure Lengend Snippet: NFIC acts on epithelial ovarian cancer through PTEN and TGFβ1. A : Western blot protein banding plots of NFIC, TBX2, PTEN, nucleus SP1, nucleus EZH2 and nucleus BRD4 as well as statistical plots of relative protein expression in NC group, NFIC-OE group, NFIC-OE + TBX2-OE group, NFIC-OE + SF1670 group and NFIC-OE + SF1670 + TGFβ1-IN-1 group; B : Western blot protein banding plots of TGFβ1, TBX3, TBX2 as well as statistical plots of relative protein expression in NC group, NFIC-OE group, NFIC-OE + TBX2-OE group, NFIC-OE + SF1670 group and NFIC-OE + SF1670 + TGFβ1-IN-1 group. GAPDH as control protein; Data are expressed as mean ± standard deviation. N = 3; ** P <0.01; * P <0.05; ns P >0.05.

Article Snippet: The PTEN inhibitor SF1670 was purchased from SELECK, and the TGFβ1 inhibitor TGFβ1-IN-1 from MCE.

Techniques: Western Blot, Expressing, Control, Standard Deviation

NFIC mediates STAT3/TGFβ1 inhibition of MMP-2 and MMP-9 expression in ovarian cancer cells. A : Western blot protein banding plots of MMP-2, and MMP-9 in NC group, NFIC-OE group, NFIC-OE + TBX2-OE group, NFIC-OE + SF1670 group and NFIC-OE + SF1670 + TGFβ1-IN-1 group; B : Statistical graph of the relative protein expression levels of MMP-2 and MMP-9 in the NC group, NFIC-OE group, NFIC-OE + TBX2-OE group, NFIC-OE + SF1670 group, and NFIC-OE + SF1670 + TGFβ1-IN-1 group. GAPDH as control protein; Data are expressed as mean ± standard deviation. N = 3; ** P <0.01; * P <0.05; ns P >0.05.

Journal: Scientific Reports

Article Title: NFIC suppressed the epithelial ovarian cancer via modulating the balance of PTEN/TGFβ1/EGR1/BRD4 and SP1/EZH2 induced Inhibition of TBX2/MMPs signaling

doi: 10.1038/s41598-025-09653-0

Figure Lengend Snippet: NFIC mediates STAT3/TGFβ1 inhibition of MMP-2 and MMP-9 expression in ovarian cancer cells. A : Western blot protein banding plots of MMP-2, and MMP-9 in NC group, NFIC-OE group, NFIC-OE + TBX2-OE group, NFIC-OE + SF1670 group and NFIC-OE + SF1670 + TGFβ1-IN-1 group; B : Statistical graph of the relative protein expression levels of MMP-2 and MMP-9 in the NC group, NFIC-OE group, NFIC-OE + TBX2-OE group, NFIC-OE + SF1670 group, and NFIC-OE + SF1670 + TGFβ1-IN-1 group. GAPDH as control protein; Data are expressed as mean ± standard deviation. N = 3; ** P <0.01; * P <0.05; ns P >0.05.

Article Snippet: The PTEN inhibitor SF1670 was purchased from SELECK, and the TGFβ1 inhibitor TGFβ1-IN-1 from MCE.

Techniques: Inhibition, Expressing, Western Blot, Control, Standard Deviation

NFIC mediates STAT3/TGFβ1 inhibition of ovarian cancer cell migration and invasion capacity. A : Diagram showing the results of the cell scratch assay for SKOV3, OVCAR-3, and A2780 cells, as well as statistical graphs of cell scratch spacing at 0 h and 48 h; B : Results of transwell invasion experiments and statistical analysis of invasive cell numbers in SKOV3, OVCAR-3, and A2780 cells. Data are expressed as mean ± standard deviation. N = 3; ** P <0.01; * P <0.05; ns P >0.05.

Journal: Scientific Reports

Article Title: NFIC suppressed the epithelial ovarian cancer via modulating the balance of PTEN/TGFβ1/EGR1/BRD4 and SP1/EZH2 induced Inhibition of TBX2/MMPs signaling

doi: 10.1038/s41598-025-09653-0

Figure Lengend Snippet: NFIC mediates STAT3/TGFβ1 inhibition of ovarian cancer cell migration and invasion capacity. A : Diagram showing the results of the cell scratch assay for SKOV3, OVCAR-3, and A2780 cells, as well as statistical graphs of cell scratch spacing at 0 h and 48 h; B : Results of transwell invasion experiments and statistical analysis of invasive cell numbers in SKOV3, OVCAR-3, and A2780 cells. Data are expressed as mean ± standard deviation. N = 3; ** P <0.01; * P <0.05; ns P >0.05.

Article Snippet: The PTEN inhibitor SF1670 was purchased from SELECK, and the TGFβ1 inhibitor TGFβ1-IN-1 from MCE.

Techniques: Inhibition, Migration, Wound Healing Assay, Standard Deviation

NFIC mediates STAT3/TGFβ1 inhibition of ovarian cancer cell proliferation. A : Western blot protein banding plots of P-PI3K, CyclinA1, CyclinD1 as well as statistical plots of relative protein expression in NC group, NFIC-OE group, NFIC-OE + TBX2-OE group, NFIC-OE + SF1670 group and NFIC-OE + SF1670 + TGFβ1-IN-1 group; B : CCK-8 assay results for SKOV3, OVCAR-3, and A2780 cells; C : Results of cloning formation experiments and statistical graphs of clone numbers for SKOV3, OVCAR-3, and A2780 cells. GAPDH as control protein; Data are expressed as mean ± standard deviation. N = 3; ** P <0.01.

Journal: Scientific Reports

Article Title: NFIC suppressed the epithelial ovarian cancer via modulating the balance of PTEN/TGFβ1/EGR1/BRD4 and SP1/EZH2 induced Inhibition of TBX2/MMPs signaling

doi: 10.1038/s41598-025-09653-0

Figure Lengend Snippet: NFIC mediates STAT3/TGFβ1 inhibition of ovarian cancer cell proliferation. A : Western blot protein banding plots of P-PI3K, CyclinA1, CyclinD1 as well as statistical plots of relative protein expression in NC group, NFIC-OE group, NFIC-OE + TBX2-OE group, NFIC-OE + SF1670 group and NFIC-OE + SF1670 + TGFβ1-IN-1 group; B : CCK-8 assay results for SKOV3, OVCAR-3, and A2780 cells; C : Results of cloning formation experiments and statistical graphs of clone numbers for SKOV3, OVCAR-3, and A2780 cells. GAPDH as control protein; Data are expressed as mean ± standard deviation. N = 3; ** P <0.01.

Article Snippet: The PTEN inhibitor SF1670 was purchased from SELECK, and the TGFβ1 inhibitor TGFβ1-IN-1 from MCE.

Techniques: Inhibition, Western Blot, Expressing, CCK-8 Assay, Cloning, Control, Standard Deviation

NFIC mediates TBX2/PTEN to promote apoptosis in ovarian cancer cells. A: Flow cytometry analysis of apoptosis in SKOV3 cells from the NC group, NFIC-OE group, NFIC-OE + TBX2-OE group, NFIC-OE + SF1670 group, and NFIC-OE + SF1670 + TGFβ1-IN-1 group; B: Statistical graph of SKOV3 cell apoptosis rate. Data are expressed as mean ± standard deviation. N = 3; ** P <0.01; * P <0.05.

Journal: Scientific Reports

Article Title: NFIC suppressed the epithelial ovarian cancer via modulating the balance of PTEN/TGFβ1/EGR1/BRD4 and SP1/EZH2 induced Inhibition of TBX2/MMPs signaling

doi: 10.1038/s41598-025-09653-0

Figure Lengend Snippet: NFIC mediates TBX2/PTEN to promote apoptosis in ovarian cancer cells. A: Flow cytometry analysis of apoptosis in SKOV3 cells from the NC group, NFIC-OE group, NFIC-OE + TBX2-OE group, NFIC-OE + SF1670 group, and NFIC-OE + SF1670 + TGFβ1-IN-1 group; B: Statistical graph of SKOV3 cell apoptosis rate. Data are expressed as mean ± standard deviation. N = 3; ** P <0.01; * P <0.05.

Article Snippet: The PTEN inhibitor SF1670 was purchased from SELECK, and the TGFβ1 inhibitor TGFβ1-IN-1 from MCE.

Techniques: Flow Cytometry, Standard Deviation

NFIC inhibits the progression of epithelial ovarian cancer by regulating the balance of PTEN/TGFβ1/EGR1/BRD4 and SP1/EZH2 to inhibit TBX2/MMPs signaling. A : Transcriptional relationship between TGFβ1 and TBX3, EGR1 expression; B : Interactions between EZH2 and HDAC3, and TBX3/TBX2/TGFβ1; C : SP1 promotes EZH2 transcription; D : NFIC promotes PTEN transcription; E: BRD4 inhibits EZH2 function.

Journal: Scientific Reports

Article Title: NFIC suppressed the epithelial ovarian cancer via modulating the balance of PTEN/TGFβ1/EGR1/BRD4 and SP1/EZH2 induced Inhibition of TBX2/MMPs signaling

doi: 10.1038/s41598-025-09653-0

Figure Lengend Snippet: NFIC inhibits the progression of epithelial ovarian cancer by regulating the balance of PTEN/TGFβ1/EGR1/BRD4 and SP1/EZH2 to inhibit TBX2/MMPs signaling. A : Transcriptional relationship between TGFβ1 and TBX3, EGR1 expression; B : Interactions between EZH2 and HDAC3, and TBX3/TBX2/TGFβ1; C : SP1 promotes EZH2 transcription; D : NFIC promotes PTEN transcription; E: BRD4 inhibits EZH2 function.

Article Snippet: The PTEN inhibitor SF1670 was purchased from SELECK, and the TGFβ1 inhibitor TGFβ1-IN-1 from MCE.

Techniques: Expressing

AZGP1 inhibited TGFβ1 induced EMT in RPE cells. Cells were treated with 10 ng/mL TGFβ1 for 48 hours to induce EMT with or without 1 µg/mL rAZGP1. ( A ) The mRNA level of AZGP1 was detected by RT-qPCR in the healthy controls, the TGFβ1, and the TGFβ1 + rAZGP1 groups in ARPE-19 cells ( N = 3). ( B , C ) Western blotting showed protein level of AZGP1 in the healthy controls, the TGFβ1, and the TGFβ1 + rAZGP1 groups in ARPE-19 cells ( N = 3 to 4). ( D – G ) Immunofluorescence staining showed reduced expression of α-SMA ( green ) with rAZGP1 treatment in ARPE-19 cells ( D , E ) and primary mouse RPE cells ( F , G ). Scale bar = 50 µm, N = 3. ( H , I ) mRNA expression of Col1a1 ( H ) and Fn1 ( I ) were detected by RT-qPCR in ARPE-19 from the healthy control, the TGFβ1, and the TGFβ1 + rAZGP1 groups ( N = 3). ( J – M ) Western blotting showed the protein expression of Fibronectin1, collagen I, and α-SMA in ARPE-19 from the healthy control, the TGFβ1, and the TGFβ1 + rAZGP1 groups ( N = 4). Control, control group; TGFβ1, TGFβ1 induction; TGFβ1 + rAZGP1, TGFβ1 induction with rAZGP1 treatment. All data are presented as mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001, the P value was obtained by 1-way ANOVA followed by multiple comparisons.

Journal: Investigative Ophthalmology & Visual Science

Article Title: AZGP1 Attenuates Subretinal Fibrosis and Inhibits Epithelial-Mesenchymal Transition by Blocking the PI3K/AKT Signaling Pathway

doi: 10.1167/iovs.66.4.83

Figure Lengend Snippet: AZGP1 inhibited TGFβ1 induced EMT in RPE cells. Cells were treated with 10 ng/mL TGFβ1 for 48 hours to induce EMT with or without 1 µg/mL rAZGP1. ( A ) The mRNA level of AZGP1 was detected by RT-qPCR in the healthy controls, the TGFβ1, and the TGFβ1 + rAZGP1 groups in ARPE-19 cells ( N = 3). ( B , C ) Western blotting showed protein level of AZGP1 in the healthy controls, the TGFβ1, and the TGFβ1 + rAZGP1 groups in ARPE-19 cells ( N = 3 to 4). ( D – G ) Immunofluorescence staining showed reduced expression of α-SMA ( green ) with rAZGP1 treatment in ARPE-19 cells ( D , E ) and primary mouse RPE cells ( F , G ). Scale bar = 50 µm, N = 3. ( H , I ) mRNA expression of Col1a1 ( H ) and Fn1 ( I ) were detected by RT-qPCR in ARPE-19 from the healthy control, the TGFβ1, and the TGFβ1 + rAZGP1 groups ( N = 3). ( J – M ) Western blotting showed the protein expression of Fibronectin1, collagen I, and α-SMA in ARPE-19 from the healthy control, the TGFβ1, and the TGFβ1 + rAZGP1 groups ( N = 4). Control, control group; TGFβ1, TGFβ1 induction; TGFβ1 + rAZGP1, TGFβ1 induction with rAZGP1 treatment. All data are presented as mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001, the P value was obtained by 1-way ANOVA followed by multiple comparisons.

Article Snippet: To induce EMT, the cells were treated with 10 ng/mL TGFβ1 (MCE, Monmouth Junction, NJ, USA), alone or in combination with human rAZGP1 protein (1 μg/mL; MCE, Monmouth Junction, NJ, USA).

Techniques: Quantitative RT-PCR, Western Blot, Immunofluorescence, Staining, Expressing, Control

AZGP1 inhibited the PI3K-AKT pathway in ARPE-19 cells. ( A ) KEGG pathway analysis showing the top 20 significant pathways of 66 common DEGs in SRF10D and SRF30D compared with the healthy controls. ( B , C ) Western blotting showed the protein expression of phospho-AKT (Ser473) and AKT in ARPE-19 from the healthy control, the TGFβ1, and the TGFβ1 + rAZGP1 groups ( N = 4). Control, control group; TGFβ1, TGFβ1 (10 ng/mL) induction for 48 hours; TGFβ1 + rAZGP1, TGFβ1 (10 ng/mL) induction with rAZGP1 (1 µg/mL) treatment for 48 hours. ( D – G ) ARPE-19 cells were transfected with negative control siRNA (NC) and Azgp1 targeted siRNA. TGFβ1 (10 ng/ml) and Capivasertib (1 µM) were added after RNA interference for additional 48 hours. Western blotting showed the phosphorylation of AKT ( D, F ) and PI3K ( E, G ) in ARPE-19 cells ( N = 3). ( H , I ) Western blotting showed the expression level of Collagen I, phosphor-AKT, AKT, phosphor-PI3K, and PI3K in ARPE-19 cells transduced with LV-Azgp1 and LV-empty after treated with 10 ng/mL TGFβ1 for 48 hours ( N = 3). The result of p-AKT/AKT was based on the band of p-AKT and AKT (incubated after stripping), whereas the result of p-PI3K/PI3K was based on the band of p-PI3K and PI3K normalized to GAPDH, respectively. All data are presented as mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001, the P value was obtained by 1-way ANOVA followed by multiple comparisons for multiple groups and two-sided t -test between individual groups.

Journal: Investigative Ophthalmology & Visual Science

Article Title: AZGP1 Attenuates Subretinal Fibrosis and Inhibits Epithelial-Mesenchymal Transition by Blocking the PI3K/AKT Signaling Pathway

doi: 10.1167/iovs.66.4.83

Figure Lengend Snippet: AZGP1 inhibited the PI3K-AKT pathway in ARPE-19 cells. ( A ) KEGG pathway analysis showing the top 20 significant pathways of 66 common DEGs in SRF10D and SRF30D compared with the healthy controls. ( B , C ) Western blotting showed the protein expression of phospho-AKT (Ser473) and AKT in ARPE-19 from the healthy control, the TGFβ1, and the TGFβ1 + rAZGP1 groups ( N = 4). Control, control group; TGFβ1, TGFβ1 (10 ng/mL) induction for 48 hours; TGFβ1 + rAZGP1, TGFβ1 (10 ng/mL) induction with rAZGP1 (1 µg/mL) treatment for 48 hours. ( D – G ) ARPE-19 cells were transfected with negative control siRNA (NC) and Azgp1 targeted siRNA. TGFβ1 (10 ng/ml) and Capivasertib (1 µM) were added after RNA interference for additional 48 hours. Western blotting showed the phosphorylation of AKT ( D, F ) and PI3K ( E, G ) in ARPE-19 cells ( N = 3). ( H , I ) Western blotting showed the expression level of Collagen I, phosphor-AKT, AKT, phosphor-PI3K, and PI3K in ARPE-19 cells transduced with LV-Azgp1 and LV-empty after treated with 10 ng/mL TGFβ1 for 48 hours ( N = 3). The result of p-AKT/AKT was based on the band of p-AKT and AKT (incubated after stripping), whereas the result of p-PI3K/PI3K was based on the band of p-PI3K and PI3K normalized to GAPDH, respectively. All data are presented as mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001, the P value was obtained by 1-way ANOVA followed by multiple comparisons for multiple groups and two-sided t -test between individual groups.

Techniques: Western Blot, Expressing, Control, Transfection, Negative Control, Phospho-proteomics, Transduction, Incubation, Stripping Membranes

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