{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‐194 (including its 5p isoform) plays diverse, context‐dependent roles in tumor biology. In several cancers—including renal cell carcinoma, non‐small cell lung cancer, colorectal cancer, osteosarcoma, esophageal carcinoma, hepatocellular carcinoma, melanoma, breast cancer, hypopharyngeal carcinoma, glioblastoma, cholangiocarcinoma, medulloblastoma, and others—the loss or reduced expression of miR‐194 is associated with enhanced proliferation, migration, invasion, and chemoresistance. Restoration of miR‐194 expression in these settings has been shown to inhibit epithelial–mesenchymal transition and tumor aggressiveness by directly targeting key oncogenic mediators such as MAP4K4, KDM5B, N‐cadherin (CDH2), IGF1R, PTBP1, SMURF1, and ROR2, among others. In contrast, in prostate cancer miR‐194 can act as a metastatic driver through suppression of SOCS2, and even within pancreatic cancer conflicting observations have been reported—with one study linking miR‐194 upregulation to tumor promotion via DACH1 suppression, and another associating higher miR‐194–5p levels with improved anti‐tumor immunity via inhibition of PD‐L1."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its tumor‐cell autonomous effects, miR‐194 also modulates multiple non‐neoplastic processes and influences the cellular response to stress. In differentiation contexts, miR‐194 promotes hepatocytic differentiation by targeting regulators such as YAP1, thereby facilitating the loss of pluripotency markers. In inflammatory settings, miR‐194 exerts anti‐inflammatory functions in conditions like psoriasis, intervertebral disc degeneration, and chronic idiopathic urticaria by regulating components of the NF‐κB and TGF‐β/SMAD pathways. Furthermore, in models of lung cell injury and deep hypothermia–induced neuronal stress, miR‐194 modulates cell viability and apoptosis through control of NF‐κB– and SUMO2–dependent signaling. Additional studies suggest that altered circulating levels of miR‐194 may serve as a predictive biomarker for chemotherapy response and disease progression in cancers such as osteosarcoma and colon cancer."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nComplex regulatory networks further fine‐tune miR‐194 activity through interactions with long non‑coding RNAs and circular RNAs that act as competing endogenous RNAs. Several studies have demonstrated that lncRNAs (for example, MALAT1, LINC00909, and H19) and circRNAs (such as circFCHO2 and circ_0000591) can “sponge” miR‐194, thereby diminishing its tumor‑suppressive effects and allowing derepression of their shared targets—key effectors involved in cell proliferation, invasion, metabolism, and signaling pathways including AKT2, ACVR2B, and HK2. These ceRNA networks underscore the critical role of miR‐194 regulation not only in cancer progression but also in modulating cellular responses to developmental and stress signals."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "25"}, {"type": "fg_f", "ref": "33"}, {"type": "fg_f", "ref": "32"}, {"type": "fg_f", "ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "H W Z Khella, M Bakhet, G Allo, et al. 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