{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nResearch over the past decade has revealed that members of the miR‐885 family—including miR‐885‐5p and miR‐885‐3p—play multifaceted, context‐dependent roles in cancer biology. In neuroblastoma, for example, ectopic expression of miR‐885‐5p induces cell cycle arrest, senescence, and apoptosis via p53 pathway activation and by targeting cell cycle regulators such as cyclin‐dependent kinase 2 (CDK2) and mini‐chromosome maintenance protein 5 (MCM5) ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "]. In squamous cell carcinoma, a cisplatin‐induced isoform—miR‐885‐3p—plays a key role in modulating apoptosis by regulating transcripts encoding proteins such as MDM4, BCL2, and several caspases ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": "]. Genetic variation that impairs miR‐885‐5p binding to targets like CASP3 further supports its importance in tumor suppression ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": "]. However, miR‐885’s functions are not uniformly suppressive. In colorectal cancer, elevated levels of miR‐885‐5p have been linked with enhanced cell migration, invasion, and epithelial–mesenchymal transition via repression of factors that normally restrain TWIST1 expression ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": "], whereas in hepatocellular carcinoma, overexpression of miR‐885‐5p is associated with decreased metastasis through downregulation of CTNNB1 and consequent inhibition of Wnt/β‐catenin signaling ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": "]. In gastric cancer, miR‐885‐3p acts as a tumor suppressor by inhibiting cyclin‐dependent kinase 4 (CDK4); notably, its activity is counteracted by oncogenic long noncoding RNAs that “sponge” miR‐885‐3p, thereby facilitating cell proliferation ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": "]. In chemoresistant lung adenocarcinoma, reduced miR‐885‐5p leads to increased Aurora A kinase expression and diminished drug sensitivity ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": "], while in cancer stem‐like cells, attenuation of miR‐885‐5p results in augmented insulin‐like growth factor 1 receptor (IGF1R) expression that supports stemness and chemoresistance ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": "]. Moreover, by targeting BMPR1A and thereby impairing Smad/Id1 signaling, miR‐885‐3p suppresses angiogenesis in colon cancer models ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": "]. Paradoxically, in certain liver tumors, miR‐885‐5p appears to promote tumorigenesis via upregulation of TIGAR through chromatin modification ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": "], and deregulation of miR‐885 activity through competing endogenous RNA (ceRNA) mechanisms is emerging as an important factor in breast and thyroid cancers ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": "].\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond oncogenesis, miR‐885 exerts significant influence in nonmalignant diseases by modulating inflammation, cellular injury, and metabolic processes. In metabolic liver disorders and during acute hepatitis C virus infection, altered circulating levels of miR‐885‐5p correlate with fatty liver development and changes in lipoprotein metabolism—possibly through regulation of lipid receptors such as oxysterol‐binding protein–like 2 (OSBPL2) ["}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "14", "end_ref": "16"}]}, {"type": "t", "text": "]. Cardioprotective roles for miR‐885‐5p have been identified in cardiomyocytes exposed to hypoxia/reoxygenation, where its upregulation attenuates apoptosis via suppression of pro‐apoptotic mediators such as PTEN and BCL2L11 and by enhancing AKT/mTOR signaling ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "17"}]}, {"type": "t", "text": "]. In immune‐mediated conditions, including asthma and cutaneous lupus erythematosus, miR‐885 regulates key receptors—such as the vitamin D receptor (VDR) and toll‐like receptor 4 (TLR4)—to dampen pro‐inflammatory NF‐κB and MyD88 signaling; genetic variants that affect its binding can thereby exacerbate disease severity ["}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "21"}]}, {"type": "t", "text": "]. Altered miR‐885 expression has also been documented in pre‐eclampsia, osteoarthritis, and cystic fibrosis, highlighting its promise as a circulating biomarker in diverse pathological states ["}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "22", "end_ref": "24"}]}, {"type": "t", "text": "]. In addition, miR‐885 participates in cellular differentiation—for instance, by post‐transcriptionally regulating dentin sialophosphoprotein (DSPP) during odontoblast maturation ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "25"}]}, {"type": "t", "text": "]—and modulates monocyte inflammatory responses in type 1 diabetes ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "26"}]}, {"type": "t", "text": "]. Epigenetic studies also indicate that changes in miR‐885 are linked with successful cognitive aging ["}, {"type": "fg", "children": [{"type": "fg_f", "ref": "27"}]}, {"type": "t", "text": "]. Finally, emerging data in prostate and ovarian cancers suggest that ceRNA networks involving long noncoding RNAs and circular RNAs can sequester miR‐885, thereby further influencing its regulatory capacity and underscoring its potential as a therapeutic target ["}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "30"}]}, {"type": "t", "text": "].\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "E A Afanasyeva, P Mestdagh, C Kumps, et al. 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