{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR-494 has emerged as a multifunctional regulator in cancer, exhibiting context‐dependent roles that can be either oncogenic or tumor suppressive. In several cancer types—including non‐small‐cell lung cancer, hepatocellular carcinoma, gliomas, and colorectal cancer—upregulation of miR-494 is associated with enhanced cell proliferation, cell cycle progression, and resistance to apoptosis, thereby contributing to tumor growth and aggressive behavior. In contrast, in malignancies such as cholangiocarcinoma, pancreatic, breast, ovarian, and gastric cancers, reduced miR-494 expression has been linked to cell cycle arrest, diminished clonogenicity, and decreased metastatic potential. These apparently divergent roles underscore the complexity of miR-494’s function in modulating tumor biology."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, miR-494 exerts its regulatory functions by directly targeting a broad spectrum of genes that are critical for cell survival, proliferation, and migration. It downregulates tumor suppressors and key cell cycle regulators—such as PTEN, CDK6, and CFTR—as well as pro-apoptotic factors including BIM. In doing so, miR-494 modulates major signaling axes like the PI3K/AKT and Wnt/β-catenin pathways and influences receptors and proteins such as nucleolin, CXCR4, and EGFR pathway mediators. These direct interactions enable miR-494 to orchestrate multiple cellular events that promote invasion and metastasis in a variety of tumor settings."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond cancer, miR-494 is implicated in a range of non-malignant conditions and may serve as both a biomarker and a therapeutic target. Its dysregulation has been observed in renal ischemia/reperfusion injury—where miR-494 suppresses ATF3 and promotes proinflammatory responses—as well as in neurodegenerative diseases; for instance, overexpression of miR-494 diminishes DJ-1 or SIRT3 levels, thereby heightening vulnerability to oxidative stress in Parkinson’s disease models. Moreover, altered miR-494 expression is linked to vascular and inflammatory processes, influencing endothelial cell function and angiogenesis, and has been detected in conditions such as interverteclal disc degeneration, pre-eclampsia, and sepsis-induced acute kidney injury. Additional studies in oral and small cell lung cancers further reveal its involvement in modulating chemosensitivity through targets like secretagogin. Together, these findings highlight the broad clinical relevance of miR-494 in both malignant and non-malignant contexts."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "27", "end_ref": "39"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Christofer Diakos, Sheng Zhong, Yuanyuan Xiao, et al. 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