{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐124, encoded by MIR124‐2 along with its related loci, is emerging as a potent tumor suppressor that plays a critical role in a variety of cancers. In hepatocellular carcinoma, pancreatic ductal adenocarcinoma, colorectal tumors, oral squamous cell carcinoma, nasopharyngeal carcinoma, and glioblastoma, miR‐124 is frequently downregulated via epigenetic mechanisms such as CpG island hypermethylation; its loss contributes to dysregulated cell proliferation, invasion, metastasis, and poor patient outcomes. Mechanistically, miR‐124 exerts its tumor‐suppressive functions by directly targeting key oncogenic drivers such as cyclin‐dependent kinases, Rac1, integrin beta‐1, splicing regulators like PTB1, DNMTs, UHRF1, and signaling molecules including Smad4. Restoring miR‐124 expression in these contexts has been shown to induce apoptosis, reverse epithelial–mesenchymal transition, and modulate critical pathways that underlie tumor progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nThe methylation status of the MIR124‐2 locus has also been harnessed as a robust biomarker in clinical diagnostics. Multiplex quantitative methylation‐specific assays that target panels including FAM19A4 and MIR124‐2 have demonstrated high sensitivity and specificity for detecting cervical cancer and its precursors. In addition, alterations in circulating levels or promoter methylation of miR‐124 have been reported in conditions such as acute stroke and pancreatic cancer, underscoring its potential utility as a noninvasive diagnostic and prognostic marker."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its intrinsic tumor‐suppressive actions, miR‐124 is subject to intricate regulation by other noncoding RNAs and intracellular signaling pathways. In several oncogenic contexts, competing endogenous RNAs such as long noncoding RNAs (for example, UCA1 and NEAT1) and circular RNAs (such as circHIPK3) act as molecular sponges to sequester miR‐124, thereby abrogating its ability to target oncogenic mediators and modulate pathways including TGF‐β signaling, metabolic reprogramming, and stemness maintenance. Furthermore, modulation of miR‐124 levels has been linked to alterations in radiosensitivity in lung cancer and to the attenuation of inflammatory signaling in mycobacterial infections. Collectively, these regulatory circuits highlight miR‐124’s central role in controlling a spectrum of cellular processes that influence cancer progression, treatment responses, and disease prognosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Mayuko Furuta, Ken-ich Kozaki, Shinji Tanaka, et al. 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