{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTranscription factor 21 (TCF21) is a basic helix‐loop‐helix transcription factor that plays a pivotal role in embryonic development, cell‐fate decisions, and tissue remodeling. Its expression is tightly controlled by epigenetic processes—for example, long noncoding RNAs such as TARID actively induce TCF21 promoter demethylation—and by interactions with growth factor and environmental signals. In the developing coronary vasculature, smooth muscle cells, kidney podocytes, and even during reproductive and endometrial differentiation, TCF21 promotes mesenchymal-to-epithelial transitions and modulates cell state by regulating key downstream effectors. In addition, genetic variants within its regulatory regions have been linked to congenital heart defects and coronary artery disease risk, while altered TCF21 expression also impacts vascular calcification processes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn a wide array of human malignancies—including lung, head and neck, breast, colorectal, gastric, renal, and melanoma as well as tumors of endocrine origin such as adrenocortical cancers—TCF21 acts as a tumor suppressor. Its expression is frequently lost as a result of promoter hypermethylation and deleterious genetic polymorphisms that disrupt microRNA binding, thereby destabilizing its transcript. Reduced TCF21 levels have been shown to enhance cell proliferation, invasion, and metastatic potential in cancer models. Moreover, mechanistic studies have revealed that TCF21 can regulate factors such as the metastasis suppressor KiSS1 and steroidogenic factor‐1 (SF‐1), which are critical for cell-cycle arrest and differentiation, suggesting that loss of TCF21 function contributes to tumor progression and an aggressive cancer phenotype."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "19", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFurther insights point to the clinical implications of TCF21 dysregulation. Altered microRNA interactions—including those mediated by circular RNAs—and genetic polymorphisms that impact TCF21 stability have been implicated in resistance to apoptosis, chemotherapy, and aberrant epithelial-to-mesenchymal transitions observed in cancers such as esophageal, ovarian, and prostate carcinoma. These studies reinforce the notion that reinstating TCF21 expression or function may not only counteract tumor aggressiveness but also serve as a prognostic indicator. Together, the expanding body of work on TCF21 underscores its potential as a therapeutic target, with restoration of its activity holding promise for improving outcomes in patients bearing TCF21-deficient tumors."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "43"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Noriko Funato, Kimie Ohyama, Takayuki Kuroda, et al. 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