{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‑429, a member of the miR‑200 family, has emerged as a multifaceted regulator in cancer biology. Extensive studies have demonstrated its pivotal role in modulating epithelial–mesenchymal transition (EMT), cell migration, invasion, and metastatic potential. In many tumor types—including colorectal, hepatocellular, cervical, thyroid, glioblastoma, renal cell, and osteosarcoma—miR‑429 functions predominantly as a tumor suppressor by targeting EMT‐promoting transcriptional repressors (e.g., ZEB1, ZEB2, Onecut2, RAB23, and CRKL) and by restoring epithelial characteristics. Conversely, in certain contexts such as non‑small cell lung cancer and prostate cancer, miR‑429 is up‑regulated and exerts oncogenic effects by down‑regulating key tumor suppressors (e.g., PTEN, RASSF8, TIMP2, and p27^Kip1), thereby promoting proliferation and metastasis."}, {"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": "\nBeyond its dichotomous role in tumorigenesis, miR‑429 modulates several key signaling pathways that are critical for cancer cell adaptation and stress responses. It contributes to the regulation of hypoxia by targeting mRNAs such as HIF1A and HIF3A—thereby influencing the switch between acute and chronic hypoxic responses—and affects viral latency by modulating host factors crucial for Epstein–Barr virus reactivation. Moreover, miR‑429 participates in determining cellular sensitivity to external stressors, including radiation, through its impact on inflammatory mediators and cytokine production, and its expression is often governed by epigenetic modifications that further influence drug sensitivity, metastatic behavior, and overall patient prognosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its well‐documented roles in cancer, miR‑429 is implicated in several non‑malignant physiological processes. It has been shown to enhance mesenchymal–epithelial transition and sensitize metastatic ovarian cancer cells to platinum‐based therapy, protect osteoblasts from glucocorticoid‑induced apoptosis via activation of AMPK, and shield cardiomyocytes against hypoxia‑induced apoptosis through Notch1 signaling. Altered miR‑429 expression has also been linked to reproductive processes and to aberrant cellular adhesion mechanisms that contribute to glioma invasion and cholangiocarcinogenesis. Overall, these findings underscore the context‑dependent and multifunctional nature of miR‑429, highlighting its potential as both a diagnostic biomarker and a therapeutic target across a diverse spectrum of human diseases."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "41"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Xiaoxia Hu, Dusten M Macdonald, Phyllis C Huettner, et al. 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