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Moreover, TWIST1 cooperates with other EMT inducers (for example, Snail2, BMI1, and PDGFRα) and downstream mediators like AKT2, vimentin via circular RNA regulation, and even Bcl‐2 to promote motile, invasive phenotypes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in EMT, TWIST1 contributes decisively to oncogenesis by enabling tumor cell survival and resistance to therapy. Studies have shown that TWIST1 can inhibit oncogene‐ and p53‐dependent apoptosis, thereby overriding failsafe mechanisms and enhancing chemoresistance. In cancers such as prostate and EGFR-mutant non–small-cell lung cancer, elevated TWIST1 correlates with increased resistance to cytotoxic drugs and targeted therapeutics. In this context, TWIST1 suppresses proapoptotic factors (for example, BIM) and collaborates with mediators such as YB-1, while also being modulated by inflammatory regulators like type I interferons."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nTWIST1 also plays key roles during embryonic development and in the regulation of stem cell fates. In normal development, its function in mesoderm specification and skeletal patterning is highlighted by its involvement in craniosynostosis and limb malformations when its dosage or dimer partner selection is altered. 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