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sox4  (Cusabio)


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    Structured Review

    Cusabio sox4
    ELF3 is a newly discovered transcription factor that regulates PES1. ( A ) The UCSC database predicts the transcription factors that may regulate PES1. ( B ) The expression of ELF3 and <t>SOX4</t> in HRMECs. Student t-test. n = 3/group. * p < 0.05 versus NG. ( C , D ) The expression of ELF3 and SOX4 in HRMECs. One-way ANOVA. n = 3/group. * p < 0.05 versus HG + NC siRNA. ( E , F ) The mRNA level of ELF3 and SOX4 in HRMECs. One-way ANOVA. n = 3/group. * p < 0.05 versus HG + NC siRNA. ( G ) Enrichment ability of ELF3 in PES1 promoter regions. Student t-test. n = 3/group. * p < 0.05 versus IgG. ( H ) Luciferase activity of PES1 promoter transfected with ELF3 overexpress plasmids or control plasmids. One-way ANOVA. n = 3/group. * p < 0.05 versus ELF3 NC group
    Sox4, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "ELF3-regulated PES1 targets VEGFR2 to mediate angiogenesis and retinal inner barrier injury in diabetic retinopathy"

    Article Title: ELF3-regulated PES1 targets VEGFR2 to mediate angiogenesis and retinal inner barrier injury in diabetic retinopathy

    Journal: Journal of Translational Medicine

    doi: 10.1186/s12967-025-07334-0

    ELF3 is a newly discovered transcription factor that regulates PES1. ( A ) The UCSC database predicts the transcription factors that may regulate PES1. ( B ) The expression of ELF3 and SOX4 in HRMECs. Student t-test. n = 3/group. * p < 0.05 versus NG. ( C , D ) The expression of ELF3 and SOX4 in HRMECs. One-way ANOVA. n = 3/group. * p < 0.05 versus HG + NC siRNA. ( E , F ) The mRNA level of ELF3 and SOX4 in HRMECs. One-way ANOVA. n = 3/group. * p < 0.05 versus HG + NC siRNA. ( G ) Enrichment ability of ELF3 in PES1 promoter regions. Student t-test. n = 3/group. * p < 0.05 versus IgG. ( H ) Luciferase activity of PES1 promoter transfected with ELF3 overexpress plasmids or control plasmids. One-way ANOVA. n = 3/group. * p < 0.05 versus ELF3 NC group
    Figure Legend Snippet: ELF3 is a newly discovered transcription factor that regulates PES1. ( A ) The UCSC database predicts the transcription factors that may regulate PES1. ( B ) The expression of ELF3 and SOX4 in HRMECs. Student t-test. n = 3/group. * p < 0.05 versus NG. ( C , D ) The expression of ELF3 and SOX4 in HRMECs. One-way ANOVA. n = 3/group. * p < 0.05 versus HG + NC siRNA. ( E , F ) The mRNA level of ELF3 and SOX4 in HRMECs. One-way ANOVA. n = 3/group. * p < 0.05 versus HG + NC siRNA. ( G ) Enrichment ability of ELF3 in PES1 promoter regions. Student t-test. n = 3/group. * p < 0.05 versus IgG. ( H ) Luciferase activity of PES1 promoter transfected with ELF3 overexpress plasmids or control plasmids. One-way ANOVA. n = 3/group. * p < 0.05 versus ELF3 NC group

    Techniques Used: Expressing, Luciferase, Activity Assay, Transfection, Control



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    ELF3 is a newly discovered transcription factor that regulates PES1. ( A ) The UCSC database predicts the transcription factors that may regulate PES1. ( B ) The expression of ELF3 and <t>SOX4</t> in HRMECs. Student t-test. n = 3/group. * p < 0.05 versus NG. ( C , D ) The expression of ELF3 and SOX4 in HRMECs. One-way ANOVA. n = 3/group. * p < 0.05 versus HG + NC siRNA. ( E , F ) The mRNA level of ELF3 and SOX4 in HRMECs. One-way ANOVA. n = 3/group. * p < 0.05 versus HG + NC siRNA. ( G ) Enrichment ability of ELF3 in PES1 promoter regions. Student t-test. n = 3/group. * p < 0.05 versus IgG. ( H ) Luciferase activity of PES1 promoter transfected with ELF3 overexpress plasmids or control plasmids. One-way ANOVA. n = 3/group. * p < 0.05 versus ELF3 NC group
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    Image Search Results


    ELF3 is a newly discovered transcription factor that regulates PES1. ( A ) The UCSC database predicts the transcription factors that may regulate PES1. ( B ) The expression of ELF3 and SOX4 in HRMECs. Student t-test. n = 3/group. * p < 0.05 versus NG. ( C , D ) The expression of ELF3 and SOX4 in HRMECs. One-way ANOVA. n = 3/group. * p < 0.05 versus HG + NC siRNA. ( E , F ) The mRNA level of ELF3 and SOX4 in HRMECs. One-way ANOVA. n = 3/group. * p < 0.05 versus HG + NC siRNA. ( G ) Enrichment ability of ELF3 in PES1 promoter regions. Student t-test. n = 3/group. * p < 0.05 versus IgG. ( H ) Luciferase activity of PES1 promoter transfected with ELF3 overexpress plasmids or control plasmids. One-way ANOVA. n = 3/group. * p < 0.05 versus ELF3 NC group

    Journal: Journal of Translational Medicine

    Article Title: ELF3-regulated PES1 targets VEGFR2 to mediate angiogenesis and retinal inner barrier injury in diabetic retinopathy

    doi: 10.1186/s12967-025-07334-0

    Figure Lengend Snippet: ELF3 is a newly discovered transcription factor that regulates PES1. ( A ) The UCSC database predicts the transcription factors that may regulate PES1. ( B ) The expression of ELF3 and SOX4 in HRMECs. Student t-test. n = 3/group. * p < 0.05 versus NG. ( C , D ) The expression of ELF3 and SOX4 in HRMECs. One-way ANOVA. n = 3/group. * p < 0.05 versus HG + NC siRNA. ( E , F ) The mRNA level of ELF3 and SOX4 in HRMECs. One-way ANOVA. n = 3/group. * p < 0.05 versus HG + NC siRNA. ( G ) Enrichment ability of ELF3 in PES1 promoter regions. Student t-test. n = 3/group. * p < 0.05 versus IgG. ( H ) Luciferase activity of PES1 promoter transfected with ELF3 overexpress plasmids or control plasmids. One-way ANOVA. n = 3/group. * p < 0.05 versus ELF3 NC group

    Article Snippet: Primary or secondary antibodies were summarized as follows: PES1(1:5000, 13553-1-AP; Proteintech, Wuhan, China; 1:100, sc-166300; Santa Cruz); VEGFA (1:1000, 19003-1-AP; Proteintech); NOX4 (1:5000, 14347-1-AP; Proteintech); VE-cadherin (1:1000, 66804-1-AP; Proteintech; 1:2000, YM8373; Immunoway, China); Occludin (1:5000, 27260-1-AP; Proteintech); SOD1 (1:10000, 10269-1-AP; Proteintech); VEGFR2 (1:1000, 26415-1-AP; Proteintech; 1:1000, R380984; Zenbio, China); ELF3 (1:1000, R389278; Zenbio); SOX4 (1:1000, CSB-PA022431LA01HU; CUSABIO, China); β-actin (1:3000, GB15003-100; Servicebio, China).

    Techniques: Expressing, Luciferase, Activity Assay, Transfection, Control

    miR-338-3p-mediated hepatic CSC self-renewal and tumor formation depend on SOX4. ( A ) Comparison of SOX4 expression in miR-338-3p knockdown against control HCC cells using RT-PCR. ( B ) left panel: SOX4 was examined by immunoblotting in miR-338-3p knockdown and untreated HCC cells. Right panel: quantification for SOX4 protein. ( C ) miR-338-3p binding sites in the 3ʹ-UTR of the SOX4 gene and the nucleotides changed in the SOX4-3ʹUTR mutant were predicted using a Target Scan. ( D ) In control HCC cells and miR-338-3p knockdown cells, the luciferase activity of the SOX4-WT or SOX4-Mut 3ʹ-UTR was assessed, and the relative activity was displayed. ( E ) Primary HCC cells ( n = 35) were analyzed using RT-PCR for their miR-338-3p and SOX4 expression levels. Spearman’s correlation analysis was performed after data were standardized to -β-actin as △Ct. ( F ) HCC cells with and without miR-338-3p knockdown were transfected with SOX4 siRNA or negative control and then cultured to generate spheroids. ( G ) Transfection of SOX4 siRNA or negative control into miR-338-3p knockdown cells and control HCC cells was then exposed to an in vitro LDA. ( H ) To perform an in vivo LDA, HCC cells expressing miR-338-3p were transfected with SOX4 siRNA or an NC. Error bars shows mean ± SD derived from n = 3 independent experiments, * p < 0.05; NS p > 0.05.

    Journal: Scientific Reports

    Article Title: miRNA-338-3p influences the liver cancer stem cells and lenvatinib resistance properties by targeting SOX4

    doi: 10.1038/s41598-025-06805-0

    Figure Lengend Snippet: miR-338-3p-mediated hepatic CSC self-renewal and tumor formation depend on SOX4. ( A ) Comparison of SOX4 expression in miR-338-3p knockdown against control HCC cells using RT-PCR. ( B ) left panel: SOX4 was examined by immunoblotting in miR-338-3p knockdown and untreated HCC cells. Right panel: quantification for SOX4 protein. ( C ) miR-338-3p binding sites in the 3ʹ-UTR of the SOX4 gene and the nucleotides changed in the SOX4-3ʹUTR mutant were predicted using a Target Scan. ( D ) In control HCC cells and miR-338-3p knockdown cells, the luciferase activity of the SOX4-WT or SOX4-Mut 3ʹ-UTR was assessed, and the relative activity was displayed. ( E ) Primary HCC cells ( n = 35) were analyzed using RT-PCR for their miR-338-3p and SOX4 expression levels. Spearman’s correlation analysis was performed after data were standardized to -β-actin as △Ct. ( F ) HCC cells with and without miR-338-3p knockdown were transfected with SOX4 siRNA or negative control and then cultured to generate spheroids. ( G ) Transfection of SOX4 siRNA or negative control into miR-338-3p knockdown cells and control HCC cells was then exposed to an in vitro LDA. ( H ) To perform an in vivo LDA, HCC cells expressing miR-338-3p were transfected with SOX4 siRNA or an NC. Error bars shows mean ± SD derived from n = 3 independent experiments, * p < 0.05; NS p > 0.05.

    Article Snippet: The siRNAs against NC siRNA and SOX4 were constructed by Ribobio (China).

    Techniques: Comparison, Expressing, Knockdown, Control, Reverse Transcription Polymerase Chain Reaction, Western Blot, Binding Assay, Mutagenesis, Luciferase, Activity Assay, Transfection, Negative Control, Cell Culture, In Vitro, In Vivo, Derivative Assay

    miR-338-3p determines the response of Lenvatinib in HCC cells. ( A ) Comparison of Lenvatinib-resistant HCC cells and control HCC cells using RT-PCR. ( B ) miR-338-3p mimic and control HCC cells were infected with a negative control virus or overexpressing SOX4 and then treated with Lenvatinib (10 µM) for 48 h. Flow cytometry was used to determine how many cells had undergone apoptosis. ( C ) K-M analysis was used to compare the overall survival of HCC patients in the miR-338-3p-high ( n = 18) and miR-338-3p-low ( n = 17) groups after treatment with Lenvatinib. Error bars shows mean ± SD derived from n = 3 independent experiments, * p < 0.05; NS p > 0.05.

    Journal: Scientific Reports

    Article Title: miRNA-338-3p influences the liver cancer stem cells and lenvatinib resistance properties by targeting SOX4

    doi: 10.1038/s41598-025-06805-0

    Figure Lengend Snippet: miR-338-3p determines the response of Lenvatinib in HCC cells. ( A ) Comparison of Lenvatinib-resistant HCC cells and control HCC cells using RT-PCR. ( B ) miR-338-3p mimic and control HCC cells were infected with a negative control virus or overexpressing SOX4 and then treated with Lenvatinib (10 µM) for 48 h. Flow cytometry was used to determine how many cells had undergone apoptosis. ( C ) K-M analysis was used to compare the overall survival of HCC patients in the miR-338-3p-high ( n = 18) and miR-338-3p-low ( n = 17) groups after treatment with Lenvatinib. Error bars shows mean ± SD derived from n = 3 independent experiments, * p < 0.05; NS p > 0.05.

    Article Snippet: The siRNAs against NC siRNA and SOX4 were constructed by Ribobio (China).

    Techniques: Comparison, Control, Reverse Transcription Polymerase Chain Reaction, Infection, Negative Control, Virus, Flow Cytometry, Derivative Assay

    A RT-PCR was used to test the mRNA levels of SOX4 in WPMY-1 and BPH-1 cells treated with TNF-α. B WB was used to test the protein levels of SOX4 in WPMY-1 and BPH-1 cells treated with TNF-α. C GEO data showing SOX4 expression in BPH samples from GSE119195 , GSE132714 , and GSE167196 . D Representative SOX4 IHC staining and quantification in normal and BPH prostate samples. E , F WB analysis of TGF-β/Smad signaling protein expression in BPH-1 and WPMY-1 cells treated with TNF-α (5 ng/mL and 10 ng/mL) for 3 days. G , H RT-PCR and WB analysis of the mRNA and protein expression of EMT markers in BPH-1 cells treated with TNF-α (5 ng/mL and 10 ng/mL) for 3 days. I , J RT-PCR and WB analysis of the mRNA and protein expression of fibrosis markers in WPMY-1 cells treated with TNF-α (5 and 10 ng/ml) for 3 days. Data are expressed as the means ± SEMs (* p < 0.05, ** p < 0.01, *** p < 0.001, ns: not significant).

    Journal: Cell Death & Disease

    Article Title: TNF-α modulates cell proliferation via SOX4/TGF-β/Smad signaling in benign prostatic hyperplasia

    doi: 10.1038/s41419-025-07783-x

    Figure Lengend Snippet: A RT-PCR was used to test the mRNA levels of SOX4 in WPMY-1 and BPH-1 cells treated with TNF-α. B WB was used to test the protein levels of SOX4 in WPMY-1 and BPH-1 cells treated with TNF-α. C GEO data showing SOX4 expression in BPH samples from GSE119195 , GSE132714 , and GSE167196 . D Representative SOX4 IHC staining and quantification in normal and BPH prostate samples. E , F WB analysis of TGF-β/Smad signaling protein expression in BPH-1 and WPMY-1 cells treated with TNF-α (5 ng/mL and 10 ng/mL) for 3 days. G , H RT-PCR and WB analysis of the mRNA and protein expression of EMT markers in BPH-1 cells treated with TNF-α (5 ng/mL and 10 ng/mL) for 3 days. I , J RT-PCR and WB analysis of the mRNA and protein expression of fibrosis markers in WPMY-1 cells treated with TNF-α (5 and 10 ng/ml) for 3 days. Data are expressed as the means ± SEMs (* p < 0.05, ** p < 0.01, *** p < 0.001, ns: not significant).

    Article Snippet: In this study, SOX4 knockdown was achieved by transducing lentiviruses containing short hairpin RNAs (shRNAs) targeting SOX4 (Sh-SOX4; Genechem, Shanghai, China) (Table ), and two shRNA sequences with better inhibition efficiency were selected for further research.

    Techniques: Reverse Transcription Polymerase Chain Reaction, Expressing, Immunohistochemistry

    A – C RT-PCR and WB were used to confirm the SOX4 knockdown effect in BPH-1 and WPMY-1 cells infected with Sh-NC or Sh-SOX4 lentivirus for 3 days. D BPH-1 and WPMY-1 cells were plated in 96-well plates (3 × 10 3 cells/well) and infected with Sh-NC or Sh-SOX4 lentivirus for 0–3 days. Cell proliferation viability was determined by CCK-8 test. E , F Flow cytometry was used to test the cells cycle of BPH-1 and WPMY-1 cells infected with Sh-NC or Sh-SOX4 lentivirus for 3 days, retrospectively. Data are expressed as the means ± SEMs (* p < 0.05, ** p < 0.01, *** p < 0.001, ns: not significant).

    Journal: Cell Death & Disease

    Article Title: TNF-α modulates cell proliferation via SOX4/TGF-β/Smad signaling in benign prostatic hyperplasia

    doi: 10.1038/s41419-025-07783-x

    Figure Lengend Snippet: A – C RT-PCR and WB were used to confirm the SOX4 knockdown effect in BPH-1 and WPMY-1 cells infected with Sh-NC or Sh-SOX4 lentivirus for 3 days. D BPH-1 and WPMY-1 cells were plated in 96-well plates (3 × 10 3 cells/well) and infected with Sh-NC or Sh-SOX4 lentivirus for 0–3 days. Cell proliferation viability was determined by CCK-8 test. E , F Flow cytometry was used to test the cells cycle of BPH-1 and WPMY-1 cells infected with Sh-NC or Sh-SOX4 lentivirus for 3 days, retrospectively. Data are expressed as the means ± SEMs (* p < 0.05, ** p < 0.01, *** p < 0.001, ns: not significant).

    Article Snippet: In this study, SOX4 knockdown was achieved by transducing lentiviruses containing short hairpin RNAs (shRNAs) targeting SOX4 (Sh-SOX4; Genechem, Shanghai, China) (Table ), and two shRNA sequences with better inhibition efficiency were selected for further research.

    Techniques: Reverse Transcription Polymerase Chain Reaction, Knockdown, Infection, CCK-8 Assay, Flow Cytometry

    A – C RT-PCR and WB were used to confirm the SOX4 overexpression effect in BPH-1 and WPMY-1 cells infected with vector or SOX4 lentivirus for 3 days. D BPH-1 and WPMY-1 cells were plated in 96-well plates (3 × 10 3 cells/well) and infected with vector or SOX4 lentivirus for 0–3 days. Cell proliferation viability was determined by CCK-8 test, respectively. E , F Flow cytometry was used to test the cells cycle of BPH-1 and WPMY-1 cells infected with vector or SOX4 lentivirus for 3 days. Data are expressed as the means ± SEMs (* p < 0.05, ** p < 0.01, *** p < 0.001, ns not significant).

    Journal: Cell Death & Disease

    Article Title: TNF-α modulates cell proliferation via SOX4/TGF-β/Smad signaling in benign prostatic hyperplasia

    doi: 10.1038/s41419-025-07783-x

    Figure Lengend Snippet: A – C RT-PCR and WB were used to confirm the SOX4 overexpression effect in BPH-1 and WPMY-1 cells infected with vector or SOX4 lentivirus for 3 days. D BPH-1 and WPMY-1 cells were plated in 96-well plates (3 × 10 3 cells/well) and infected with vector or SOX4 lentivirus for 0–3 days. Cell proliferation viability was determined by CCK-8 test, respectively. E , F Flow cytometry was used to test the cells cycle of BPH-1 and WPMY-1 cells infected with vector or SOX4 lentivirus for 3 days. Data are expressed as the means ± SEMs (* p < 0.05, ** p < 0.01, *** p < 0.001, ns not significant).

    Article Snippet: In this study, SOX4 knockdown was achieved by transducing lentiviruses containing short hairpin RNAs (shRNAs) targeting SOX4 (Sh-SOX4; Genechem, Shanghai, China) (Table ), and two shRNA sequences with better inhibition efficiency were selected for further research.

    Techniques: Reverse Transcription Polymerase Chain Reaction, Over Expression, Infection, Plasmid Preparation, CCK-8 Assay, Flow Cytometry

    A Valcano plot showing the differentiated expressed genes in WPMY-1 cells knocking down SOX4. B GO analysis showing pathways down/up-regulated in WPMY-1 cells knocking down SOX4. C Enrichment plots of GSEA analyses for significant pathways in Sh-SOX4 group compared with Sh-NC group in WPMY-1 cells. D , E WB analysis of TGF-β/Smad pathway protein expression in BPH-1 and WPMY-1 cells infected with Sh-NC or Sh-SOX4 lentivirus for 3 days. F , G RT-PCR and WB analysis of EMT marker expression in BPH-1 cells infected with Sh-NC or Sh-SOX4 lentivirus for 3 days. H , I RT-PCR and WB analysis of fibrosis marker expression in WPMY-1 cells infected with Sh-NC or Sh-SOX4 lentivirus for 3 days. J WPMY-1 cells were plated in 96-well plates (3 × 10 3 cells/well) overnight. Then, WPMY-1 cells were pretreated with TNF-α and transfected with SOX4 lentivirus for 3 days. Cells viability was determined by CCK-8 test. K WB showing SOX4 and TGF-β1 protein expression in WPMY-1 cells treated with TNF-α and infected with Sh-SOX4 lentivirus for 3 days. Data are expressed as the means ± SEMs (* p < 0.05, ** p < 0.01, *** p < 0.001, ns: not significant).

    Journal: Cell Death & Disease

    Article Title: TNF-α modulates cell proliferation via SOX4/TGF-β/Smad signaling in benign prostatic hyperplasia

    doi: 10.1038/s41419-025-07783-x

    Figure Lengend Snippet: A Valcano plot showing the differentiated expressed genes in WPMY-1 cells knocking down SOX4. B GO analysis showing pathways down/up-regulated in WPMY-1 cells knocking down SOX4. C Enrichment plots of GSEA analyses for significant pathways in Sh-SOX4 group compared with Sh-NC group in WPMY-1 cells. D , E WB analysis of TGF-β/Smad pathway protein expression in BPH-1 and WPMY-1 cells infected with Sh-NC or Sh-SOX4 lentivirus for 3 days. F , G RT-PCR and WB analysis of EMT marker expression in BPH-1 cells infected with Sh-NC or Sh-SOX4 lentivirus for 3 days. H , I RT-PCR and WB analysis of fibrosis marker expression in WPMY-1 cells infected with Sh-NC or Sh-SOX4 lentivirus for 3 days. J WPMY-1 cells were plated in 96-well plates (3 × 10 3 cells/well) overnight. Then, WPMY-1 cells were pretreated with TNF-α and transfected with SOX4 lentivirus for 3 days. Cells viability was determined by CCK-8 test. K WB showing SOX4 and TGF-β1 protein expression in WPMY-1 cells treated with TNF-α and infected with Sh-SOX4 lentivirus for 3 days. Data are expressed as the means ± SEMs (* p < 0.05, ** p < 0.01, *** p < 0.001, ns: not significant).

    Article Snippet: In this study, SOX4 knockdown was achieved by transducing lentiviruses containing short hairpin RNAs (shRNAs) targeting SOX4 (Sh-SOX4; Genechem, Shanghai, China) (Table ), and two shRNA sequences with better inhibition efficiency were selected for further research.

    Techniques: Expressing, Infection, Reverse Transcription Polymerase Chain Reaction, Marker, Transfection, CCK-8 Assay

    A , B WB analysis of SOX4 protein expression in BPH-1 and WPMY-1 cells treated with Met (0, 5, and 10 mM), retrospectively. C BPH-1 and WPMY-1 cells were plated in 96-well plates (3 × 10 3 cells/well) overnight. Then, BPH-1 and WPMY-1 cells were treated with doses of Met (0, 1, 5, 10, and 20 mM) for different time points (0, 24, 48, and 72 h). Cells viability was determined by CCK-8 test. D BPH-1 and WPMY-1 cells were plated in 6-well plates (2 × 10 5 cells/well) overnight. Then, BPH-1 and WPMY-1 cells treated with Met (0, 5, and 10 mM) for 3 days, and harvested for cell cycle test via flow cytometry. E , F WB analysis of TGF-β/Smad pathway protein expression in BPH-1 and WPMY-1 cells treated with Met (0, 5, and 10 mM) for 3 days. G WB analysis of EMT marker expression in BPH-1 cells treated with Met (0, 5, and 10 mM) for 3 days. H WB analysis of fibrosis marker expression in WPMY-1 cells treated with Met (0, 5, and 10 mM) for 3 days. Data are expressed as the means ± SEMs (* p < 0.05, ** p < 0.01, *** p < 0.001, ns: not significant).

    Journal: Cell Death & Disease

    Article Title: TNF-α modulates cell proliferation via SOX4/TGF-β/Smad signaling in benign prostatic hyperplasia

    doi: 10.1038/s41419-025-07783-x

    Figure Lengend Snippet: A , B WB analysis of SOX4 protein expression in BPH-1 and WPMY-1 cells treated with Met (0, 5, and 10 mM), retrospectively. C BPH-1 and WPMY-1 cells were plated in 96-well plates (3 × 10 3 cells/well) overnight. Then, BPH-1 and WPMY-1 cells were treated with doses of Met (0, 1, 5, 10, and 20 mM) for different time points (0, 24, 48, and 72 h). Cells viability was determined by CCK-8 test. D BPH-1 and WPMY-1 cells were plated in 6-well plates (2 × 10 5 cells/well) overnight. Then, BPH-1 and WPMY-1 cells treated with Met (0, 5, and 10 mM) for 3 days, and harvested for cell cycle test via flow cytometry. E , F WB analysis of TGF-β/Smad pathway protein expression in BPH-1 and WPMY-1 cells treated with Met (0, 5, and 10 mM) for 3 days. G WB analysis of EMT marker expression in BPH-1 cells treated with Met (0, 5, and 10 mM) for 3 days. H WB analysis of fibrosis marker expression in WPMY-1 cells treated with Met (0, 5, and 10 mM) for 3 days. Data are expressed as the means ± SEMs (* p < 0.05, ** p < 0.01, *** p < 0.001, ns: not significant).

    Article Snippet: In this study, SOX4 knockdown was achieved by transducing lentiviruses containing short hairpin RNAs (shRNAs) targeting SOX4 (Sh-SOX4; Genechem, Shanghai, China) (Table ), and two shRNA sequences with better inhibition efficiency were selected for further research.

    Techniques: Expressing, CCK-8 Assay, Flow Cytometry, Marker

    A WPMY-1 cells were plated in 96-well plates (3 × 10 3 cells/well) overnight. Then, WPMY-1 cells were treated with Vector, Vector combined with Met, overexpression SOX4, or overexpression SOX4 combined with Met. for different time points (0, 24, 48, and 72 h). Cells viability was determined by CCK-8 test. B , C WPMY-1 cells were plated in 6-well plates (2 × 10 5 cells/well) overnight. Then, WPMY-1 cells were treated with Vector, Vector combined with Met, overexpression SOX4, or overexpression SOX4 combined with Met for 3 days, and harvested for cell cycle test via flow cytometry. D WPMY-1 cells were plated in 6-well plates (2 × 10 5 cells/well) overnight. Then, WPMY-1 cells were treated with Vector, Vector combined with Met, overexpression SOX4, or overexpression SOX4 combined with Met for 3 days, and harvested for cell apoptosis test via flow cytometry. Data are expressed as the means ± SEMs (* p < 0.05, ** p < 0.01, *** p < 0.001).

    Journal: Cell Death & Disease

    Article Title: TNF-α modulates cell proliferation via SOX4/TGF-β/Smad signaling in benign prostatic hyperplasia

    doi: 10.1038/s41419-025-07783-x

    Figure Lengend Snippet: A WPMY-1 cells were plated in 96-well plates (3 × 10 3 cells/well) overnight. Then, WPMY-1 cells were treated with Vector, Vector combined with Met, overexpression SOX4, or overexpression SOX4 combined with Met. for different time points (0, 24, 48, and 72 h). Cells viability was determined by CCK-8 test. B , C WPMY-1 cells were plated in 6-well plates (2 × 10 5 cells/well) overnight. Then, WPMY-1 cells were treated with Vector, Vector combined with Met, overexpression SOX4, or overexpression SOX4 combined with Met for 3 days, and harvested for cell cycle test via flow cytometry. D WPMY-1 cells were plated in 6-well plates (2 × 10 5 cells/well) overnight. Then, WPMY-1 cells were treated with Vector, Vector combined with Met, overexpression SOX4, or overexpression SOX4 combined with Met for 3 days, and harvested for cell apoptosis test via flow cytometry. Data are expressed as the means ± SEMs (* p < 0.05, ** p < 0.01, *** p < 0.001).

    Article Snippet: In this study, SOX4 knockdown was achieved by transducing lentiviruses containing short hairpin RNAs (shRNAs) targeting SOX4 (Sh-SOX4; Genechem, Shanghai, China) (Table ), and two shRNA sequences with better inhibition efficiency were selected for further research.

    Techniques: Plasmid Preparation, Over Expression, CCK-8 Assay, Flow Cytometry

    A Prostate pictures in control, BPH, and BPH combined with Met groups, retrospectively. B Representative HE staining of prostate samples in control, BPH, and BPH combined with Met group. C Bar plots showing the body weight, prostate weight, and prostate index in control, BPH, and BPH combined with Met groups. D Bar plots showing the serum levels of TNF-α, IL-1β, and IL-6 in control, BPH, and BPH combined with Met groups. E Representative SOX4 IHC staining of prostate samples in control, BPH, and BPH combined with Met groups. F Representative IHC staining of Ki-67 in prostate samples from the control, BPH, and BPH combined with Met groups. G Representative Masson staining of prostate samples from the control, BPH, and BPH combined with Met groups. Data are expressed as the means ± SEMs (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns not significant).

    Journal: Cell Death & Disease

    Article Title: TNF-α modulates cell proliferation via SOX4/TGF-β/Smad signaling in benign prostatic hyperplasia

    doi: 10.1038/s41419-025-07783-x

    Figure Lengend Snippet: A Prostate pictures in control, BPH, and BPH combined with Met groups, retrospectively. B Representative HE staining of prostate samples in control, BPH, and BPH combined with Met group. C Bar plots showing the body weight, prostate weight, and prostate index in control, BPH, and BPH combined with Met groups. D Bar plots showing the serum levels of TNF-α, IL-1β, and IL-6 in control, BPH, and BPH combined with Met groups. E Representative SOX4 IHC staining of prostate samples in control, BPH, and BPH combined with Met groups. F Representative IHC staining of Ki-67 in prostate samples from the control, BPH, and BPH combined with Met groups. G Representative Masson staining of prostate samples from the control, BPH, and BPH combined with Met groups. Data are expressed as the means ± SEMs (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns not significant).

    Article Snippet: In this study, SOX4 knockdown was achieved by transducing lentiviruses containing short hairpin RNAs (shRNAs) targeting SOX4 (Sh-SOX4; Genechem, Shanghai, China) (Table ), and two shRNA sequences with better inhibition efficiency were selected for further research.

    Techniques: Control, Staining, Immunohistochemistry