Alternative splicing downstream of EMT enhances phenotypic plasticity and malignant behavior in colon cancer.

ABSTRACT: Phenotypic plasticity allows carcinoma cells to transiently acquire the quasi-mesenchymal features necessary to detach from the primary mass and proceed along the invasion-metastasis cascade. A broad spectrum of epigenetic mechanisms is likely to cause the epithelial-to-mesenchymal (EMT) and mesenchymal-to-epithelial (MET) transitions necessary to allow local dissemination and distant metastasis. Here, we report on the role played by alternative splicing (AS) in eliciting phenotypic plasticity in epithelial malignancies with focus on colon cancer. By taking advantage of the coexistence of subpopulations of fully epithelial (EpCAM^hi) and quasi-mesenchymal and highly metastatic (EpCAM^lo) cells in conventional human cancer cell lines, we here show that the differential e

SUBMITTER: Xu T 

PROVIDER: S-EPMC9674345 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature