Abstract
Epithelial-mesenchymal transition (EMT) is a crucial event in appropriate embryonic development as well as in wound healing, tissue repair and cancer progression in adult tissues. EMT endows cells with migratory and invasive properties, inhibits apoptosis and senescence, contributes to immunosuppression and induces stress resistance and stem cell properties. Many secreted polypeptide factors act in a sequential or cooperative manner to elicit EMT. Transforming growth factor (TGF)-β can initiate and maintain EMT by activating intracellular signalling pathways. Recent studies have provided new insights into molecular mechanisms by which TGF-β mediates changes in transcription of EMT regulators and EMT marker proteins, as well as changes in alternative splicing controlled by epithelial splicing regulatory proteins 1 and 2. Here, we present some of the emerging molecular mechanisms that mediate EMT upon exposure to TGF-β.
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