{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐421 (miR-421) has emerged as a critical regulatory molecule that is frequently dysregulated in multiple human diseases. In several studies, miR-421 was found to modulate key DNA damage response and cell cycle checkpoint proteins—for example, it suppresses ATM expression, thereby altering the S‐phase checkpoint and increasing radiosensitivity, while its overexpression induced by oncogenic factors such as N‐Myc contributes to neuroblastoma tumorigenesis. In gastric cancer, altered miR-421 expression has been investigated for its potential biomarker value, and in pancreatic cancer it targets the tumor suppressor DPC4/Smad4, promoting proliferation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistic investigations have revealed that miR-421 directly targets several genes pivotal for the regulation of cell death, differentiation, and stress responses. It downregulates proteins such as ACE2, FXR, FOXO4, caspase-3, and PDCD4—thereby promoting oncogenic phenotypes like enhanced proliferation, migration, invasion, resistance to apoptosis, and chemoresistance in cancers including gastric, biliary tract, nasopharyngeal, and osteosarcoma. Moreover, by repressing regulators such as SERPINE1 and modulating apoptotic mediators in various tumor types, miR-421 exhibits a multifaceted role; its targeting of molecules like TMEM48 in lung cancer and caspase-10 in breast cancer further underscores its capacity to influence divergent cellular pathways."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its direct regulatory functions in tumor cells, miR-421 holds promise as a circulating biomarker and therapeutic target. In various malignancies—including gastric, prostate, and thyroid cancers—as well as in non-neoplastic conditions like metabolic syndrome and even in pigmentary disorders such as vitiligo, dysregulated expression of miR-421 correlates with disease progression, metastasis, and treatment resistance. Furthermore, miR-421 is subject to modulation by competing endogenous RNAs such as circular RNAs and long noncoding RNAs (e.g., circDHRS3, lncRNA SNHG1, and circ_C16orf62), which sponge miR-421 and thereby indirectly influence the expression of downstream targets. Intriguingly, while miR-421 often exhibits oncogenic properties, in certain contexts—such as in subsets of breast, lung, and cervical cancers—it can exert tumor-suppressive effects via targeting anti-apoptotic factors or oncogenes. Collectively, these findings underscore the complex, context-dependent roles of miR-421 in regulating cell proliferation, apoptosis, migration, inflammation, and chemoresistance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "34"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Hailiang Hu, Liutao Du, Gindy Nagabayashi, et al. 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