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Alternative Splicing During Epithelial-Mesenchymal Transition (EMT)

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Sendurai Mani, PhD

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Description: Alternative splicing activates mesenchymal-specific phenotypes by regulating splicing factors. ESRP1 governs epithelial splicing of NUMB, CD44, and others, while shorter or alternative variants promote mesenchymal states. RMB47 regulates MAP37K in epithelial splicing. RBFOX2, SRSF1, QKI, and FOXP1 drive E/M hybrid and mesenchymal-like states. Adapted from Figure 6 of the article 'Spatial and Temporal Relationship between Epithelial–Mesenchymal Transition (EMT) and Stem Cells in Cancer'.

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Alternative splicing activates mesenchymal-specific phenotypes by regulating splicing factors. ESRP1 governs epithelial splicing of NUMB, CD44, and others, while shorter or alternative variants promote mesenchymal states. RMB47 regulates MAP37K in epithelial splicing. RBFOX2, SRSF1, QKI, and FOXP1 drive E/M hybrid and mesenchymal-like states. Adapted from Figure 6 of the article 'Spatial and Temporal Relationship between Epithelial–Mesenchymal Transition (EMT) and Stem Cells in Cancer'.

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