{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐296 (miR‐296) has emerged as a multifunctional regulator in non‐neoplastic contexts. For example, during enterovirus 71 infection miR‐296‐5p is upregulated and acts directly on viral genomic sequences to inhibit replication, suggesting an important role in host antiviral defence. In addition, miR‐296 regulates vascular and renal homeostasis: it modulates hWNK4 expression in a cell‐specific manner—potentially impacting blood pressure regulation—and its loss, often via sequestration by sponging circular RNAs, contributes to diabetic renal fibrosis by permitting increased expression of proteins such as the sodium–glucose cotransporter SGLT2. Moreover, in models of osteoarthritis, downregulation of miR‐296 (particularly the ‐3p form) is associated with enhanced chondrocyte apoptosis and extracellular matrix catabolism through modulation of pathways such as TGF‑β1/CTGF/p38MAPK."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": ""}, {"type": "p", "children": [{"type": "t", "text": "\nIn multiple human cancers the miR‐296 family generally exhibits tumor‐suppressive functions. In parathyroid carcinoma and esophageal squamous cell cancer, decreased miR‐296 levels have been reported, suggesting that loss of miR‐296 contributes to malignant transformation. In prostate cancer, miR‐296‐5p directly targets Pin1 while in breast cancer its downregulation correlates with aberrant expression and mis‐localization of the cell‐polarity protein Scrib, each event being linked to enhanced tumor progression. Similar antiproliferative, anti‐migratory and anti‐stemness effects are observed in non–small cell lung cancer (NSCLC), triple‐negative breast cancer (via a ceRNA axis that regulates PLK1), clear cell renal cell carcinoma (by targeting SOX12) and hepatocellular carcinoma (through a Brg1/Sall4 axis). In nasopharyngeal carcinoma, miR‐296‐3p suppresses metastasis by targeting MK2 and modulating Ras/PI3K/Akt signaling, while in choroidal melanoma and certain colorectal and pancreatic cancers miR‐296 downregulation correlates with tumor aggressiveness. Moreover, in papillary thyroid carcinoma and cholangiocarcinoma, recent studies have demonstrated that deregulation of miR‐296—often by long noncoding RNA or circular RNA “sponges” (for example, AGAP2‐AS1, circPLK1 or circ_0000515)—perturbs key signaling pathways, thereby diminishing its suppressive control over oncogenic targets."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "30"}, {"type": "fg_f", "ref": "3"}, {"type": "fg_f", "ref": "31"}, {"type": "fg_f", "ref": "4"}, {"type": "fg_f", "ref": "33"}]}, {"type": "t", "text": ""}, {"type": "p", "children": [{"type": "t", "text": "\nConversely, context‐dependent and even oncogenic functions have been reported for miR‐296. In immortalized cells, miR‐296 overexpression has been implicated in the suppression of p53 activity via targeting of the p21 3′‑UTR, thereby contributing to carcinogenesis. In certain glioblastoma models, the miR‐296‐5p isoform promotes invasiveness by directly inhibiting pro‑apoptotic and differentiation‐promoting targets such as caspase‑8 and the nerve growth factor receptor. In another glioma study, aberrantly high levels of miR‐296‑3p were found to downregulate inhibitors of the β‑catenin pathway (for instance, ICAT), thereby releasing oncogenic Wnt signaling and fostering aggressive cell cycle progression. These findings underscore that the net impact of miR‐296 on tumor biology depends on the cellular context and the balance of its interactions with various sponging noncoding RNAs and mRNA targets."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "35", "end_ref": "37"}, {"type": "fg_f", "ref": "29"}, {"type": "fg_f", "ref": "38"}]}]}]}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jinyuan Mao, Chunyi Li, Yuanyuan Zhang, et al. 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