{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐495 exhibits context‐dependent functions in cancer, acting predominantly as a regulator of cell proliferation, migration, invasion, apoptosis, and treatment response. In several malignancies—including prostate cancer, where its downregulation correlates with metastasis; breast cancer stem cells, in which its upregulation promotes colony formation and tumor growth; acute myeloid leukemia, where its reinstatement impairs MLL‐fusion–mediated transformation; gastric and non–small cell lung cancers, where it suppresses oncogenic factors such as PRL‐3, ATP7A, and MTA3; as well as colorectal, endometrial, and bladder cancers where its enforced expression inhibits tumor progression—miR‐495 functions as a tumor suppressor by directly targeting key oncogenes (e.g., FOXC1, FAM83D, and CDK6) and modulators of drug‐resistance. Its differential expression in these studies supports its dual role in oncogenesis, where, in some contexts, elevated miR‐495 expression can also contribute to cancer stem cell survival and chemoresistance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its roles in modulating oncogenic processes, miR‐495 has been implicated in the regulation of chemoresistance and in the complex interplay with long noncoding and circular RNAs that serve as molecular sponges. For example, in gastric and nasopharyngeal carcinomas, miR‐495 targeting of GRP78 improves drug sensitivity and radiosensitivity, while in clear cell renal cell carcinoma and gastric cancer, competitive binding by lncRNAs such as LUCAT1, SNHG20, or LINC01320 reduces miR‐495 availability and thereby derepresses oncogenic targets like SATB1, ZFX, or RAB19. In non–small cell lung cancer, the sequestration of miR‐495 by UCA1 contributes to cisplatin resistance via modulation of NRF2. These findings emphasize the therapeutic potential of restoring or mimicking miR‐495 activity to overcome drug resistance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond oncology, miR‐495 plays pivotal roles in non‐malignant contexts where its dysregulation influences inflammation, tissue differentiation, and cardiovascular pathology. Its modulation has been linked to endothelial cell proliferation and survival in atherosclerosis, the inhibition of cardiac fibrosis under high‐glucose conditions, and regulation of apoptosis in inflammatory bowel disease. Similarly, altered miR‐495 expression in circulating exosomes has emerged as a potential early biomarker for pre‐eclampsia, while in sepsis and septic acute kidney injury, miR‐495 influences inflammatory responses and endoplasmic reticulum stress. Furthermore, inhibition of miR‐495 enhances the generation of endothelial cells from human induced pluripotent stem cells, thereby promoting neovascularization and functional recovery following myocardial infarction, and its regulation in intervertebral disc cells suggests a protective role against disc degeneration."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "W W Hwang-Verslues, P-H Chang, P-C Wei, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "miR-495 and miR-551a inhibit the migration and invasion of human gastric cancer cells by directly interacting with PRL-3."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cancer Lett (2012)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.canlet.2012.03.029"}], "href": "https://doi.org/10.1016/j.canlet.2012.03.029"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "22469786"}], "href": "https://pubmed.ncbi.nlm.nih.gov/22469786"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Xi Jiang, Hao Huang, Zejuan Li, et al. 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