CYMP-AS1 Promotes Ovarian Cancer Progression by Enhancing the Intracellular Translocation of hnRNPM and Reducing the Stability of AXIN2 mRNA.

CYMP-AS1 通过增强 hnRNPM 的细胞内转位和降低 AXIN2 mRNA 的稳定性来促进卵巢癌的进展

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作者:Wang Yuhan, Meng Yimei, Xia Wanqiu, Liang Yusen, Wang Yaru, Li Peiling, Fang Lei
BACKGROUND: Ovarian cancer (OC) is a representative malignancy of the female reproductive system, with a poor prognosis. Long non-coding RNAs (lncRNAs) crucially affect tumor development. This study aimed to identify lncRNAs that potentially participated in OC. METHODS: LncRNA expression in cells and tissues was quantified using reverse transcription-quantitative PCR, while fluorescence in situ hybridization determined their cellular localization. Various in vitro assays, together with a mouse xenograft model, were employed to elucidate the function of CYMP antisense RNA 1 (CYMP-AS1) in OC. The molecular mechanisms underlying CYMP-AS1 regulation were investigated through RNA pull-down and immunoprecipitation assays, immunofluorescence staining, western blotting, and mRNA stability assays. RESULTS: This study identified a previously unreported lncRNA, CYMP-AS1, which exhibits increased expression in the cytoplasm of OC tissues and cells. Knockout of CYMP-AS1 reduced the OC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). CYMP-AS1 directly interacts with heterogeneous nuclear ribonucleoprotein M (hnRNPM), inducing its intracellular translocation and reducing the stability of Axis inhibition protein 2 (AXIN2) mRNA. This process ultimately elevated the expression of Wnt/β-catenin signaling pathway-related proteins. CONCLUSION: This study confirms CYMP-AS1 as a novel biomarker in OC progression and suggests that the CYMP-AS1/hnRNPM/AXIN2 axis may offer an innovative strategy for OC treatment.

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