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The Epithelial–mesenchymal transition (EMT) regulatory network is a complex signaling system that enables polarized epithelial cells to undergo biochemical changes, resulting in a mesenchymal phenotype characterized by enhanced migratory capacity and invasiveness (Lamouille et al., 2014, Nature Reviews Molecular Cell Biology). This network is essential for normal physiological processes such as embryonic development and wound healing, but its dysregulation is a hallmark of cancer metastasis and organ fibrosis (Nieto et al., 2016, Cell). In oncology, the EMT program contributes to tumor heterogeneity, immune evasion, and resistance to chemotherapy and radiation (Dongre & Weinberg, 2019, Nature Reviews Molecular Cell Biology). Therapeutic strategies targeting this network focus on inhibiting key upstream signaling molecules like TGF-beta, Notch, and Wnt, or downstream transcription factors such as Snail, Twist, and Zeb (PubMed, PMID: 27339105). While targeting the EMT network holds promise for preventing metastasis, challenges include the high plasticity of the process and the potential for adverse effects on normal tissue repair and homeostasis (PubMed, PMID: 30546054).
Inhibition of TGF-beta signaling, STAT3 inhibition, Wnt pathway modulation, and antagonism of EMT-inducing transcription factors.
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