ArticleAmerican journal of translational research2024
CTEN-induced TGF-β1 expression facilitates EMT and enhances paclitaxel resistance in bladder cancer cells.
Article in American journal of translational research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- TGF‑β1 in cancer: From tumour suppressor to promoter, molecular mechanisms, and precision therapeutic strategies (Review).International journal of oncology · 2026Review
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6 authors.
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Abstract
objectivesTo investigate the role of C-terminal tensin-like (CTEN) in mediating chemotherapy resistance via epithelial-mesenchymal transition (EMT) in bladder cancer (BC) cells, through the regulation of transforming growth factor-β1 (TGF-β1) expression.
methodsLentiviral vectors were used to create CTEN overexpression and knockdown constructs, which were then introduced into paclitaxel-resistant BC cell lines. The effects of CTEN manipulation on cell proliferation and drug sensitivity was assessed using the CCK-8 assay, and apoptosis was evaluated by flow cytometry. The expression levels of CTEN, TGF-β1, and EMT markers were quantified by RT-qPCR and Western blot analysis. The interaction between CTEN and TGF-β1 and its effect on TGF-β1 methylation were studied using bisulfite sequencing PCR and co-immunoprecipitation.
resultsOverexpression of CTEN in BC cells was associated with decreased paclitaxel efficacy, reduced apoptosis, and elevated levels of TGF-β1 and EMT-related proteins. CTEN was found to bind TGF-β1, inhibiting its methylation and thereby promoting TGF-β1 upregulation. This increase in TGF-β1 expression facilitated the EMT process and enhanced drug resistance in BC cells.
conclusionsThe induction of TGF-β1 expression by CTEN promotes EMT and increases chemotherapy resistance in BC cells. Targeting CTEN or the EMT pathway could improve chemosensitivity in treatment-resistant BC, suggesting a novel therapeutic strategy to enhance chemotherapy effectiveness.
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