{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe long non‐coding RNA PVT1, located at the 8q24 chromosomal region, frequently undergoes copy‑number gain and is co‑amplified with the adjacent MYC oncogene in a wide array of human cancers. Such genomic alterations contribute to elevated MYC protein levels and enhanced tumorigenicity in malignancies ranging from hepatocellular carcinoma and colorectal to gallbladder cancer. In addition, both the linear and circular (circPVT1) isoforms of PVT1 are markedly overexpressed in these tumors, a change that correlates with aggressive clinicopathologic characteristics and poor patient prognosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, PVT1 exerts its oncogenic effects through diverse pathways. Its transcription can be induced in a p53‑dependent manner while the PVT1 locus also engages in promoter competition with MYC, thereby influencing MYC transcription. Moreover, the PVT1 transcript enhances tumor cell proliferation and invasion by stabilizing key oncogenic proteins through interactions with chromatin modifiers such as EZH2, FOXM1, NOP2, and KAT2A. PVT1 and its circular isoform furthermore act as competing endogenous RNAs (ceRNAs) by “sponging” tumor‐suppressive microRNAs—including let‑7, miR‑146a, miR‑200b, and others—thus disinhibiting critical cell cycle and anti‑apoptotic regulators. Additional studies demonstrate that PVT1 regulates transcription in a developmental and allele‑specific manner, and that its genomic promoter region itself can harbor tumor‑suppressive functions when mutated."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its direct oncogenic roles, PVT1 contributes to chemoresistance, metabolic reprogramming, and intercellular communication. In pancreatic and gastric cancer models, altered PVT1 expression modulates responses to drugs such as gemcitabine and paclitaxel by rewiring signaling networks that govern apoptosis and cell cycle progression. In osteosarcoma, for instance, PVT1 sponges miR‑497 to upregulate key glycolytic enzymes, thereby promoting aerobic glycolysis, while exosomal transfer of PVT1 between bone marrow mesenchymal and tumor cells further fuels tumor growth and metastasis. Genomic rearrangements involving PVT1 have been documented in multiple myeloma, and specific splice variants (e.g. PVT1‑214) have been implicated in reinforcing stem‑like properties in colorectal cancer. Finally, emerging evidence links PVT1 to non‑malignant pathologies including diabetic nephropathy and even the regulation of ferroptosis during brain ischemia–reperfusion injury."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "30", "end_ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yinghui Guan, Wen-Lin Kuo, Jackie L Stilwell, et al. 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