Publications by authors named "Win-Yan Liu-Bordes"

Article Synopsis
  • - Epithelial-to-mesenchymal transition (EMT) is a process that helps cancer cells spread (metastasize) and become resistant to cell death and treatments, but the triggers for EMT are not well understood
  • - The study shows that DNA damage activates specific proteins (PARP and ALC1), which help EMT transcription factors access DNA, leading to changes in cell behavior and enhanced ability to repair DNA
  • - Using a PARP inhibitor can reverse or prevent EMT caused by DNA damage, and help make cancer cells more sensitive to other treatments, offering potential new strategies for cancer therapy
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TWIST1 is a basic helix-loop-helix transcription factor, and one of the master Epithelial-to-Mesenchymal Transition (EMT) regulators. We show that tumor suppressor miR-145-5p controls TWIST1 expression in an immortalized prostate epithelial cell line and in a tumorigenic prostate cancer-derived cell line. Indeed, shRNA-mediated miR-145-5p silencing enhanced TWIST1 expression and induced EMT-associated malignant properties in these cells.

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Background: Most carcinomas are composed of heterogeneous populations of tumor cells with distinct and apparently stable phenotypic characteristics.

Methods: Using an in vitro model of carcinogenesis we aimed at experimentally elucidating the significance of heterogeneity in the expression of CD24, a marker frequently overexpressed in various cancers and correlated with poor prognosis.

Results: We show that CD24 and CD24 cells issued from the same tumorigenic cell line display striking differences in stem-related properties, expression of epithelial-mesenchymal transition/mesenchymal-epithelial transition markers, and tumorigenic capacity.

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