{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMIR330, which exists as both the 3p and 5p mature forms, has emerged as a critical regulator in diverse biological processes, most notably in cancer. In several malignancies such as prostate, colorectal, and pancreatic cancers, reduced MIR330 expression exerts tumor‐suppressive effects by directly targeting key oncogenic mediators. For instance, in prostate cancer decreased MIR330 levels relieve inhibition of E2F1 and SP1—thereby promoting Akt phosphorylation and cell survival—and in colorectal cancer MIR330 negatively regulates oncogenes like Cdc42 and ITGA5, resulting in cell cycle arrest and apoptosis. Similar inhibitory roles have been observed in pancreatic cancer, acute myeloid leukemia, and even in inflammatory skin disorders like psoriasis, where MIR330 targets CTNNB1 to restrict keratinocyte proliferation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn contrast, context‐dependent studies indicate that MIR330 can also assume oncogenic properties. In glioblastoma stem cells and certain non‐small cell lung and pancreatic cancer models, overexpression of the MIR330 3p strand has been linked to enhanced proliferation, migration, and resistance to apoptosis. For example, elevated MIR330 expression in lung cancer has been shown to promote metastasis by targeting hSOD2, while in other settings its upregulation facilitates cell cycle progression through downregulation of EGR2. Moreover, in oesophageal adenocarcinoma, attenuation of MIR330‐5p is associated with subtle increases in radiotherapy resistance—highlighting the pleiotropic and context‐dependent functions of this microRNA."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its intrinsic functions, MIR330 activity is frequently modulated by interactions with long noncoding RNAs and circular RNAs, which act as molecular sponges to sequester MIR330 and thereby influence downstream oncogenic or tumor‐suppressive pathways. In melanoma, laryngeal, cervical, and ovarian cancers—as well as in non‐small cell lung and bladder cancers—such sponging by diverse circRNAs (e.g. circ_102179, circSEMA5A, circ_0000517) and lncRNAs (e.g. EWSAT1) leads to altered expression of targets including NOB1, S100A7, and RIPK4, ultimately affecting proliferation, epithelial–mesenchymal transition, and metastatic behavior. In addition, genetic variants affecting MIR330 regulation have been implicated in psychiatric mood and anxiety traits, and in nonmalignant conditions such as atherosclerosis and psoriasis MIR330 modulates inflammatory signaling cascades. Together, these studies underscore the nuanced, context‐dependent roles of MIR330 in governing cellular growth, differentiation, and stress responses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "K-H Lee, Y-L Chen, S-D Yeh, et al. 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