{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nStudies across multiple malignancies have revealed that miR‑374a (and its mature isoform miR‑374a‑5p) plays context‐dependent roles in tumor biology. In certain cancers, such as metastatic breast cancer, gastric cancer, esophageal cancer, ovarian cancer, bladder cancer, pancreatic cancer, and triple‐negative breast cancer, elevated miR‑374a levels promote malignant phenotypes by enhancing epithelial–mesenchymal transition, cell proliferation, invasion, and metastasis through activation of oncogenic pathways (for example, Wnt/β‑catenin, PI3K/AKT, and STAT3 signaling) via direct targeting of key negative regulators such as WIF1, PTEN, CCND1, and TGFA. Conversely, in colon adenocarcinoma and lung adenocarcinoma, miR‑374a overexpression has been shown to suppress tumor progression by inactivating the PI3K/AKT axis and inhibiting pro‑growth mediators."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to influencing malignancy per se, miR‑374a has been implicated in modulating resistance to therapy. In non–small cell lung cancer, for instance, miR‑374a—under the regulatory influence of oncogenic receptor kinases such as Axl—affects gefitinib resistance by altering key cell cycle regulators and epithelial–mesenchymal transition characteristics. Similarly, in esophageal squamous cell carcinoma, ceRNA interactions involving lncRNA LINC00473 modulate radioresistance via reciprocal regulation with miR‑374a‑5p. Experimental models in pancreatic cancer and glioma further suggest that manipulating miR‑374a levels may sensitize tumor cells to chemotherapeutic and radiotherapeutic agents."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "14", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond cancer, miR‑374a exerts significant functions in non‑malignant conditions and cellular homeostasis. In vascular and inflammatory contexts, for example, this microRNA regulates endothelial responses by binding to the 3′‑UTR of PBEF/NAMPT and mitigating inflammatory signaling. It also protects retinal pigment epithelial cells against oxidative stress–induced apoptosis via targeting Fas, while in renal systems, exosomal delivery of miR‑374a‑5p has been shown to attenuate fibrosis through modulation of the MAPK6/MK5/YAP axis. Furthermore, miR‑374a‑5p participates in neural stem cell differentiation by repressing Hes1 and also appears to modulate inflammatory responses in conditions such as inflammatory bowel disease, osteoarthritis, and even in metabolic adaptations seen in obesity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, emerging evidence underscores the complexity of miR‑374a regulation through competing endogenous RNA networks. Long non‑coding RNAs such as lnc‑FTX, MAGI2‑AS3, and LINC‑PINT have been shown to sequester miR‑374a, thereby relieving repression of targets like PTEN and ARRB1 and ultimately modulating tumor progression. Similarly, circular RNAs—for example, circMETTL15—act as sponges for miR‑374a‑5p, affecting downstream effectors such as ESCO2. 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