{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‐200c is emerging as a master regulator of epithelial identity and a potent suppressor of epithelial–mesenchymal transition (EMT) in diverse cancers. By directly targeting transcriptional repressors such as ZEB1, TCF8, and regulators like WAVE3, miR‐200c restores E‐cadherin expression, thereby reinforcing cell–cell adhesion and promoting an epithelial phenotype. Its forced expression in breast, lung, prostate, bladder, and claudin‐low breast cancer models has been shown to inhibit cell invasion, diminish stem‐like properties, and reduce tumorigenicity and metastatic potential. Moreover, miR‐200c’s action in these settings highlights its capacity to modulate cytoskeletal organization and interfere with pathways that drive cancer cell plasticity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its role in suppressing EMT, miR‐200c considerably influences therapeutic responsiveness. By targeting key mediators such as FAP‐1 and regulators of drug efflux and survival signaling, miR‐200c sensitizes cancer cells to apoptotic stimuli and reverses resistance to chemotherapeutic agents, targeted therapies (e.g. trastuzumab in HER2‐positive tumors) and radiotherapy. Preclinical evidence in breast, melanoma, and osteosarcoma models supports that restoring miR‐200c expression can diminish drug resistance and improve intracellular drug accumulation, thereby enhancing treatment efficacy. 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