{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTMPO‐AS1 is an oncogenic long noncoding RNA that is aberrantly overexpressed in a wide range of malignancies—including breast cancer, non–small cell lung cancer (NSCLC), colorectal, ovarian, esophageal, osteosarcoma, retinoblastoma, cholangiocarcinoma, and bladder cancer—and is frequently associated with poor clinical prognosis. In estrogen receptor–positive breast cancer, for example, TMPO‐AS1 is induced by estrogen and promotes cell proliferation and endocrine therapy resistance by stabilizing ESR1 mRNA, whereas in NSCLC it is concomitantly overexpressed with its sense transcript TMPO, enhancing TMPO mRNA stability via antisense pairing. Comprehensive analyses have underscored its widespread oncogenic functions and its correlation with unfavorable patient outcomes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, TMPO‐AS1 exerts its oncogenic role by functioning as a competing endogenous RNA that sequesters several tumor‐suppressive microRNAs, thereby derepressing downstream oncogenes and key proliferative pathways. For instance, in osteosarcoma TMPO‐AS1 sponges miR‐199a‐5p to upregulate WNT7B and activate the Wnt/β‐catenin pathway"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": ", while in ovarian cancer it prevents miR‐200c–mediated inhibition of TMEFF2, leading to PI3K/Akt pathway activation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": " In lung and colorectal cancers, TMPO‐AS1 sequesters miR‐143‐3p, which results in the upregulation of cell cycle regulators such as CDK1."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": " Moreover, it can interact with transcription regulators—binding to FUS and recruiting p300 to the TMPO promoter in esophageal squamous cell carcinoma, and associating with E2F6 to enhance LCN2 transcription in ovarian cancer."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}, {"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFurther expanding its functional repertoire, TMPO‐AS1 also modulates key oncogenic and hypoxia–responsive pathways in other tumor types. In retinoblastoma, it regulates the expression of hypoxia–inducible factor–1α"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": ", and in cholangiocarcinoma it sponges let‐7g–5p to increase HMGA1 expression, promoting cell proliferation and migration."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": " Its oncogenic influence is further observed in bladder cancer and colorectal cancer, where TMPO‐AS1 knockdown suppresses cell proliferation, migration, and invasion."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "13"}]}, {"type": "t", "text": " Notably, emerging evidence even implicates TMPO‐AS1 in benign ovary disorders such as polycystic ovary syndrome, thereby broadening its functional spectrum."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": " Collectively, these findings highlight TMPO‐AS1 as a multifunctional regulator that modulates mRNA stability, acts as a molecular sponge for various microRNAs, and enlists transcriptional co‐activators to facilitate tumorigenesis and chemoresistance."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}, {"type": "fg_fs", "start_ref": "13", "end_ref": "15"}, {"type": "fg_f", "ref": "12"}, {"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Zhiming Qin, Xiangru Zheng, Yu Fang "}, {"type": "b", "children": [{"type": "t", "text": "Long noncoding RNA TMPO-AS1 promotes progression of non-small cell lung cancer through regulating its natural antisense transcript TMPO."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Biochem Biophys Res Commun (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.bbrc.2019.06.088"}], "href": "https://doi.org/10.1016/j.bbrc.2019.06.088"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "31230752"}], "href": "https://pubmed.ncbi.nlm.nih.gov/31230752"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Yuichi Mitobe, Kazuhiro Ikeda, Takashi Suzuki, et al. 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