{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐629 (MIR629) has emerged as a multifaceted regulator implicated in a broad spectrum of diseases. In inflammatory and immune‐mediated disorders, altered miR‑629 levels have been observed: for example, in pediatric systemic lupus erythematosus, elevated miR‑629 expression correlates with increased disease activity and inflammatory markers, while in asthma, global miRNA profiling suggests that miRNAs—including miR‑629—might help distinguish disease phenotypes. In addition, several studies exploring miRNA‐based biomarkers in malignancies such as triple‑negative breast cancer and pancreatic cancer hint at the clinical potential of circulating miR‑629 for noninvasive diagnostics and disease monitoring."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFunctional investigations in numerous cancers have established an oncogenic role for miR‑629 by directly targeting key tumor suppressors and thereby promoting proliferation, invasion, and metastasis. In lung cancer, miR‑629 modulates NBS1 expression by binding to a polymorphic site in its 3′‑UTR, and in clear cell renal cell carcinoma, it regulates the TGFβ/Smad signaling cascade via direct targeting of TRIM33. Similarly, in ovarian and pancreatic carcinomas, miR‑629 enhances cellular proliferation and invasiveness through the suppression of TSPYL5 and FOXO3, respectively; in colorectal cancer, its upregulation leads to decreased expression of CXXC4. Other studies have documented miR‑629’s ability to downregulate SFTPC in lung adenocarcinoma, its dual promotion of tumor invasion via PPWD1 and CELSR1 in lung adenocarcinoma, and its pro‑oncogenic actions in hepatocellular carcinoma through SFRP2 targeting. In prostate cancer, miR‑629 supports proliferation by diminishing LATS2 levels, and in chronic myeloid leukemia, its elevated expression in extracellular vesicles is associated with imatinib resistance. Moreover, in osteosarcoma, increased miR‑629 levels suppress CAV1 expression, collectively underpinning a broad tumor‑promoting role."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its oncogenic functions, miR‑629 also operates in non‑tumor settings, where it modulates vascular cell behavior and extracellular matrix dynamics. In pulmonary arterial hypertension, for instance, hypoxia‑induced upregulation of miR‑629 in pulmonary artery smooth muscle cells promotes proliferation and migration by targeting regulators such as FOXO3 and PERP. In calcified aortic valve disease, miR‑629‑3p exerts anti‑calcification effects by targeting TAGLN, suggesting a role in modulating calcification processes and vascular remodeling."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nThe regulatory action of miR‑629 is intricately modulated by interactions with other non‑coding RNAs that function as molecular sponges or competitive inhibitors. In cervical cancer, for example, the circular RNA circNRIP1 sequesters miR‑629‑3p to modulate PTP4A1/ERK1/2 signaling and thereby influence tumor progression. Similarly, in osteosarcoma, the long non‑coding RNA MIR22HG binds miR‑629‑5p to relieve suppression of TET3, while in clear cell renal cell carcinoma, MAGI2‑AS3 attenuates miR‑629‑5p–mediated repression of PRDM16. In addition, studies in non‑small‑cell lung cancer underscore the complex regulatory environment—highlighting both miR‑629’s potential functional roles and its emerging utility as a circulating biomarker."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "22"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jia Zhu, Xiaolan Huang, Gaixiu Su, et al. 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