{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐365A displays context‐dependent functions in tumor biology by acting either as a tumor suppressor or, in some settings, as an oncogenic microRNA. In several malignancies—including colon, non–small cell lung, cervical, breast, liver, glioma, and gallbladder cancers—miR‐365A is frequently downregulated, and its restoration can inhibit cell cycle progression, reduce proliferation, induce apoptosis, and ultimately suppress tumor growth through direct targeting of key oncogenic drivers such as Cyclin D1, Bcl‐2, thyroid transcription factor‑1 (TTF‑1), PIK3R3, ADAMTS‑1, and other effectors involved in oncogenic signaling pathways. These studies also show that low miR‑365A expression is associated with advanced disease stage and poor prognosis, and that its re‐expression may sensitize tumor cells to standard therapies."}, {"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": "\nConversely, in other cancer types the functional role of miR‑365A appears to be oncogenic. For example, in pancreatic ductal adenocarcinoma and cutaneous squamous cell carcinoma, high miR‑365A levels promote chemoresistance and tumor progression by targeting pro‑apoptotic proteins such as BAX and adaptor molecules like SHC1, while also modulating the expression of factors involved in cell survival (for instance via regulation of NFIB, TET1, and other downstream effectors). Studies in non–small cell lung cancer, triple‑negative breast cancer, laryngeal cancer, osteosarcoma, and even in melanoma—where its function has been described as controversial—further indicate that overexpression of miR‑365A can enhance metastatic potential, confer drug resistance (including resistance to gefitinib via modulation of PELI3 and TRIM25), and support a more aggressive tumor phenotype."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "14", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond cancer, miR‑365A also plays important roles in non‑malignant processes. It acts as a critical regulator of inflammatory responses—negatively modulating interleukin‑6 production—and mediates effects of mechanical stress in osteoarthritis by targeting histone deacetylase 4, thereby contributing to cartilage catabolism. In endothelial cells, miR‑365A potentiates oxidized low‑density lipoprotein–induced apoptosis by regulating Bcl‑2, while in bone and cartilage biology it influences osteogenic differentiation and stem cell function. Moreover, miR‑365A has been shown to modulate cardiac repolarization by targeting key ion channels and is even detectable as a circulating marker correlated with glycemic control in patients with type 1 diabetes. Finally, in immune cells its levels can be modulated by long non‑coding RNAs (for example, NEAT1 acting as a sponge in dendritic cells in systemic lupus erythematosus) to impact pro‑inflammatory cytokine production."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "27", "end_ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jing Nie, Lin Liu, Wei Zheng, et al. 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