{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRecent investigations have revealed that the miR‐490 family (encompassing both miR‐490‐3p and miR‐490‐5p) is aberrantly expressed in a wide range of human tissues and malignancies. For example, in uterine leiomyoma, deregulation of miR‐490 was identified, while in hepatocellular carcinoma (HCC) miR‐490‐3p was found up‐regulated where it surprisingly promoted cell proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT) by enhancing the expression of ERGIC3 in an Ago2‐dependent manner. In addition, enforced expression of miR‐490‐5p in bladder cancer cells induced G1‐phase arrest by directly targeting the oncogene c‐Fos, and in lung cancer models, miR‐490‐3p overexpression led to reduced proliferation via inhibition of CCND1. Likewise, in ovarian carcinoma, increased miR‐490‐3p induced cell cycle arrest and apoptosis by directly targeting CDK1, thereby curtailing tumorigenesis and progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn contrast to these oncogenic roles, several studies have demonstrated potent tumor‐suppressive functions for miR‐490 in diverse cancers. In osteosarcoma, restoration of miR‐490‐3p diminished cell proliferation and tumorigenicity by down‐regulating HMGA2; similarly, its down‐regulation in renal cell carcinoma has been noted, although its precise function therein remains to be fully elucidated. In colorectal and endometrial cancers, reduced miR‐490‐3p levels are associated with enhanced invasiveness and metastasis, with direct targeting of key regulators such as TGF‑β1 mediating growth inhibition. Moreover, in HCC and triple‐negative breast cancer, miR‐490 attenuates oncogenic signaling by targeting regulators such as E2F2, ECT2, TNKS2, and other mediators, leading to increased apoptosis and suppression of invasion. Additional studies further showed that in HCC models miR‐490‐3p targeting ATG7 curtailed autophagy‐related proliferation, while in colorectal carcinoma direct repression of RAB14 contributed to tumor suppression. Finally, in another HCC study, miR‐490‐5p inhibited cell migration and invasion by down‐regulating ROBO1, and suppression of vasculogenic mimicry in triple‐negative breast cancer was achieved via targeting TWIST1."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its direct regulation of cell proliferation and survival, miR‐490 is embedded in complex competing endogenous RNA (ceRNA) networks that further modulate its function. In HCC, for instance, lncRNA CCAT1 “sponges” miR‐490‐3p to relieve its suppression on CDK1, thus facilitating cell proliferation and invasion. Similarly, in thoracic ossification of the ligamentum flavum, miR‐490‐3p suppresses osteogenic differentiation via direct targeting of FOXO1. In esophageal squamous cell and pharyngolaryngeal carcinomas, miR‐490‐3p contributes to the regulation of EMT by targeting MAP3K9. In prostate cancer, miR‐490‐3p exerts tumor‐suppressive actions by repressing HDAC2, whereas lncRNA‐mediated sequestration of miR‐490 leads to FRAT1 up‐regulation. In cholangiocarcinoma, negative regulation of Akirin2 by miR‐490‐3p limits angiogenesis and metastasis, and in acute myeloid leukemia, miR‐490‐3p is sequestered by CCAT1 to activate the MAPK1/c‐Myc axis. Furthermore, in atherosclerosis, Linc00299 binds miR‐490‐3p to up‐regulate AURKA, promoting vascular smooth muscle proliferation; in glioblastoma, miR‐490 modulates telomere maintenance via targeting shelterin and telomere‐associated proteins (TERF2, TNKS2, SMG1); and in non‐small cell lung cancer, lncRNA CCDC144NL‑AS1 impairs miR‐490‐3p activity, facilitating tumor progression. Finally, in prostate and colorectal cancers, ceRNA interactions involving CCAT1 and subsequent targeting of FRAT1, IRAK1, FUT1, and GPRIN2 underpin correlations with patient outcomes, while in pancreatic cancer miR‐490‐5p impedes invasion by targeting MAGI2‐AS3 and modulating EMT."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "19", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Boryana Georgieva, Ivan Milev, Ivan Minkov, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "miR-490-3p modulates cell growth and epithelial to mesenchymal transition of hepatocellular carcinoma cells by targeting endoplasmic reticulum-Golgi intermediate compartment protein 3 (ERGIC3)."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Biol Chem (2013)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1074/jbc.M112.410506"}], "href": "https://doi.org/10.1074/jbc.M112.410506"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "23212913"}], "href": "https://pubmed.ncbi.nlm.nih.gov/23212913"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Shiqi Li, Xianglai Xu, Xin Xu, et al. 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