ArticleCancer gene therapy2025
ALKBH5-mediated m6A regulates the alternative splicing events of SRSF10 in ovarian cancer.
Article in Cancer gene therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- ALKBH5 promotes ovarian cancer progression by activating Notch2 signaling.Biological procedures online · 2026Article
- RNA Regulatory Networks: Key Hubs in the Panorama of Cancer and Emerging Therapeutic Targets.MedComm · 2026Review
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11 authors.
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Abstract
N6-methyladenosine (m6A) methylation was found to be involved in the tumorigenesis and development of ovarian cancer. Until now, it is not clear to identify the mechanism by m6A demethylase ALKBH5 affects RNA splicing in ovarian cancer. In this study, we examined ALKBH5 protein expression and m6A levels by immunohistochemistry and analyzed their correlation with clinical features and prognosis in patients with ovarian cancer. We identified the elevated expression of ALKBH5 and a general reduction in the level of m6A in ovarian cancer patients. In the ovarian cancer cell line A2780, ALKBH5 depletion was found using the siRNA strategy or the CRISPR/Cas9 knockout (KO) method, which significantly reduced the level of m6A and inhibited cell viability, proliferation, and migration. The MeRIP-seq and RNA-seq showed that ALKBH5-regulated m6A RNA modification mainly affects RNA splicing function in ovarian cancer cells. SRSF10 is a key target gene involved in alternative splicing regulation through ALKBH5-m6A. ALKBH5 knockdown resulted in increased retention of SRSF10 exon 5 and decreased expression of transcript SRSF10-211. In conclusion, the alternative splicing regulation effect by ALKBH5-mediated m6A suggests a novel promising approach for m6A modification in OC and provides novel insights into the mechanisms involved in ovarian cancer therapy.
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