{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐573 (miR‐573) has emerged as a critical regulator in diverse malignancies. In melanoma, reduced miR‐573 levels lead to enhanced expression of melanoma cell adhesion molecule (MCAM), thereby facilitating tumor progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In gastric and pancreatic cancers, miR‐573 directly targets TSPAN1 to suppress cell proliferation, invasion, and migration."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": " In prostate cancer, its downregulation is correlated with increased fibroblast growth factor receptor 1 (FGFR1) expression and enhanced epithelial–mesenchymal transition, promoting metastasis"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": ", while in hepatocellular carcinoma, overexpression of miR‐573 suppresses apolipoprotein M (apoM), reducing apoptosis via modulation of Bcl2A1 and ultimately favoring tumor growth."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": " Moreover, miR‐573 modulates ARHGAP26 expression through its 3′‐UTR, where ADAR1‐mediated A‐to‐I RNA editing prevents miR‐573 binding and affects RhoA activity."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its roles in solid tumors, miR‐573 contributes to the orchestration of angiogenic and proliferative signaling in various cancer subtypes and inflammatory conditions. In familial breast cancers, downregulation of miR‐573 is linked to disturbances in focal adhesion, VEGF, and HIF‐1 signaling pathways."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": " In cervical and non‐small cell lung cancers, competing endogenous RNAs—such as lncRNA TTN‐AS1 and FLVCR1‐AS1—sequester miR‐573, which normally represses oncogenic E2F3, thereby promoting cell proliferation and invasion."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": " A similar sponging mechanism is observed in breast cancer, where SNHG1 reduces miR‐573 levels to increase LMO4 expression and drive oncogenic behavior."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": " In rheumatoid arthritis, miR‐573 directly targets TXNDC5—and novel targets such as EGFR and TLR2—to inhibit key inflammatory mediators and angiogenic factors, thereby exerting a protective effect against joint inflammation and vascular remodeling."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond oncogenesis and inflammation, miR‐573 plays important roles in tissue homeostasis and vascular integrity. Its function in intervertebral disc biology has been probed, with investigations suggesting a protective role in degenerative nucleus pulposus cells."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": " Moreover, during dengue virus infection, miR‐573 is significantly downregulated in endothelial cells—a change associated with increased ANGPT2 expression and vascular permeability; restoration of miR‐573 mitigates endothelial dysfunction by suppressing ANGPT2 and dampening TLR2‐mediated inflammatory interferon responses."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": " Finally, emerging research into circRNA regulation in melanoma further highlights the intricate non‐coding RNA networks within which miR‐573 operates."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": " Collectively, these findings establish miR‐573 as a multifaceted regulator that can function as a tumor suppressor or, in certain contexts, contribute to tumor progression and inflammatory pathology by modulating diverse signaling pathways.\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "He-Fei Wang, Hong Chen, Min-Wang Ma, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "TSPAN1 functions as an oncogene in gastric cancer and is downregulated by miR-573."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "FEBS Lett (2015)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.febslet.2015.05.044"}], "href": "https://doi.org/10.1016/j.febslet.2015.05.044"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "26054975"}], "href": "https://pubmed.ncbi.nlm.nih.gov/26054975"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Lei Wang, Peng Gao, Ping Yuan, et al. 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