{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nVPS9D1‐AS1, also known as MYU, has emerged as an important long non‐coding RNA whose overexpression contributes to tumorigenesis in diverse malignancies. In colon cancer, VPS9D1‐AS1 acts as a direct target of c‐Myc and drives cell proliferation by interacting with hnRNP‐K to stabilize CDK6 expression, while its elevated levels in colorectal cancer are associated with poor prognosis. In hepatocellular carcinoma, VPS9D1‐AS1 binds to the HuR protein, thereby enhancing the stability of CDK4 mRNA and promoting tumor growth; furthermore, a functional polymorphism in VPS9D1‐AS1 has been shown to affect its binding with miR‑361‑3p and correlate with the clinical stage of colorectal tumors."}, {"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": "\nIn prostate cancer and other solid tumors such as non‐small cell lung, ovarian, and endometrial cancers, VPS9D1‐AS1 functions predominantly as an oncogene by serving as a competitive endogenous RNA. In prostate cancer, distinct studies report that VPS9D1‐AS1 promotes cell growth and migration by upregulating c‑Myc through sponging miR‑184 and by modulating the miR‑4739/MEF2D as well as miR‑187‑3p/FGFRL1 axes. In non‐small cell lung cancer, heightened expression correlates with lymph node metastasis and reduced survival. Similarly, in ovarian cancer, VPS9D1‐AS1 sequesters miR‑6827‑5p to elevate HMGA1 expression, and in endometrial cancer it sustains tumorigenesis via the miR‑187‑3p/S100A4 axis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its role in solid tumors, VPS9D1‐AS1 also contributes to hematologic malignancies. In acute lymphoblastic leukemia, for instance, it promotes cell proliferation through a competing endogenous RNA mechanism that modulates the miR‑491‑5p/miR‑214‑3p/GPX1 axis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yoshihiro Kawasaki, Mimon Komiya, Kosuke Matsumura, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "Long non-coding RNA MYU promotes prostate cancer proliferation by mediating the miR-184/c-Myc axis."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Oncol Rep (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.3892/or.2018.6661"}], "href": "https://doi.org/10.3892/or.2018.6661"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30132573"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30132573"}]}, {"type": "r", "ref": 6, "children": [{"type": "t", "text": "Xiaobin Wang, Qiangjun Chen, Xi Wang, et al. 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