{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐194‐1 plays multifaceted roles in cancer, where its expression and effects vary by tumor type. In several malignancies—including metastatic renal cell carcinoma, non‐small cell lung cancer, colorectal cancer, hepatocellular carcinoma, osteosarcoma, gastric cancer, laryngeal carcinoma, clear cell kidney carcinoma, prostate cancer and certain pancreatic ductal adenocarcinomas—miR‐194‐1 has been shown to modulate cell cycle progression, migration, invasion and apoptosis. In many of these contexts, restoration of miR‐194‐1 expression suppresses tumor growth and metastasis by directly targeting key oncogenic factors such as MDM2, FOXA1, MAP4K4, RBX1, SOCS2, Wee1, PTBP1 and others, while in distinct settings (for example, in prostate cancer and specific PDAC cases) its elevated levels can promote a more aggressive phenotype. These findings indicate that miR‐194‐1 may function either as a tumor suppressor or, in a tissue‐dependent manner, may contribute to oncogenic processes by altering the balance of its downstream effectors."}, {"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": "\nBeyond its direct impact on neoplastic cell behavior, miR‐194‐1 regulates differentiation and shapes the tumor microenvironment through intricate cross‐talk with other noncoding RNAs. Reduced miR‐194‐1 expression is associated with enhanced chondrogenesis of adipose‐derived stem cells (via derepression of SOX5), whereas its upregulation promotes hepatocytic differentiation by targeting YAP1 in liver progenitor cells and modulates myogenic differentiation by relieving inhibition of BCLAF1. In addition, miR‐194‐1 contributes to anti–tumor immunity, for instance, by downregulating PD‐L1 expression in pancreatic cancer, and its availability is further modulated via sponging by competing endogenous RNAs such as H19, NEAT1 and linc‐ROR as well as being subject to regulation by tumor suppressors like p53. Moreover, in psoriasis, miR‐194‐1 directly targets GRHL2, thereby balancing keratinocyte proliferation and differentiation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "14", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn non‐neoplastic conditions, miR‐194‐1 also plays critical roles in modulating inflammatory and metabolic responses. Its downregulation is linked to the pathogenesis of diabetic nephropathy and fatty acid–mediated inflammation through targeting TRAF6, while in intervertebral disc degeneration, reduced miR‐194‐1 expression permits the upregulation of ubiquitin ligase components (CUL4A/B) in response to proinflammatory cytokines. Moreover, in autosomal dominant polycystic kidney disease, the loss of miR‐194‐1 contributes to cyst expansion via deregulation of epithelial–mesenchymal transition effectors, and its altered levels in circulating extracellular vesicles highlight its potential as a noninvasive biomarker in lung adenocarcinoma. Evidence from hepatitis B virus models further underscores that miR‐194‐1 modulates apoptotic responses by targeting key anti‐apoptotic proteins."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "29"}]}, {"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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