{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMIR362, encompassing both the –3p and –5p species, has emerged as a highly versatile regulator in cancer biology. In several solid tumors, its dysregulated expression has been linked to either oncogenic or tumor‐suppressive functions. For instance, MIR362 can promote ferroptosis in tumor cells by modulating key effectors such as MIOX via a competing endogenous RNA mechanism (NEAT1/miR‐362–3p) and, in other contexts, act as an oncomiR by activating pathways such as NF‐κB via inhibition of CYLD. In contrast, in breast, neuroblastoma, renal, cervical, and osteosarcoma models, MIR362–3p has been shown to impede cell proliferation, migration, invasion and to promote apoptosis by targeting proteins including p130Cas, Tob2, and factors involved in epithelial–mesenchymal transition as well as the IL6ST/JAK2/STAT3 axis. Moreover, its expression is controlled by upstream epigenetic and long non‐coding RNA regulators—including CASC2, FENDRR, MALAT1, and SBF2‐AS1—which further modulate its downstream effects on key signaling components such as GRB2 and Sema3A."}, {"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 addition to its roles in tumor cell biology, MIR362 functions in a variety of non‐cancer contexts by fine‐tuning cellular signaling and homeostasis. In immune cells, for example, MIR362–5p enhances natural killer cell cytotoxicity by down‐regulating negative regulators of NF‐κB signaling. Vascular smooth muscle proliferation and migration in atherosclerosis are inhibited via direct targeting of ADAMTS1, while in cardiomyocytes and trophoblastic as well as neural cells, MIR362 modulates responses to hypoxia/reoxygenation injury and influences neurodevelopmental processes. Furthermore, recent studies in colon carcinoma models have demonstrated that MIR362–5p regulates iron influx by targeting the iron transporter SLC11A2, and circRNA networks in colorectal cancer modulate glycolysis and malignant behaviors through binding to MIR362–5p. A complex interplay between MIR362 and additional non‐coding RNAs and pseudogene transcripts further supports its role as a critical node in diverse signaling networks."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "19", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nEmerging evidence also points to the potential utility of MIR362 as a diagnostic and prognostic biomarker in various clinical settings. Aberrant levels of MIR362 in circulating blood, as well as in purified tumor cells, have been associated with cytogenetically normal acute myeloid leukemia and breast cancer subtypes, highlighting its promise as a molecular marker for disease stratification and therapeutic guidance."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jin-tang Xia, Lian-zhou Chen, Wei-hua Jian, et al. 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