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Epithelial-Mesenchymal Transition (EMT)-Induced Treatment Resistance

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Sendurai Mani, PhD

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Description: EMT promotes therapy resistance by activating signaling in cancer stem cells and hybrid E/M cells. SNAI1/2 inhibit p53-mediated apoptosis, enhancing chemo- and radioresistance. MIR200 downregulation regulates EMT and stemness, while EMT inducers upregulate ABC transporters, aiding chemotherapy evasion. Adapted from Figure 4 of Spatial and Temporal Relationship between Epithelial–Mesenchymal Transition (EMT) and Stem Cells in Cancer.

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EMT promotes therapy resistance by activating signaling in cancer stem cells and hybrid E/M cells. SNAI1/2 inhibit p53-mediated apoptosis, enhancing chemo- and radioresistance. MIR200 downregulation regulates EMT and stemness, while EMT inducers upregulate ABC transporters, aiding chemotherapy evasion. Adapted from Figure 4 of Spatial and Temporal Relationship between Epithelial–Mesenchymal Transition (EMT) and Stem Cells in Cancer.

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