ArticleCell proliferation2025
RBM39 Promotes Base Excision Repair to Facilitate the Progression of HCC by Stabilising OGG1 mRNA.
Article in Cell proliferation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Phosphorylation of RBM39 by CDK13 stabilizes RAD50 mRNA to drive cisplatin resistance in endometrial cancer.The Journal of biological chemistry · 2026Article
- RNA-binding motif proteins as context-dependent regulators of tumor-immune crosstalk, genome stability, and therapeutic vulnerabilities in cancer.Frontiers in immunology · 2026Review
- RBM39 Promotes Base Excision Repair to Facilitate the Progression of HCC by Stabilising OGG1 mRNA.Cell proliferation · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
Targeting base excision repair (BER) has been an attractive strategy in cancer therapeutics. RNA-binding motif protein 39 (RBM39) modulates the alternative splicing of numerous genes involved in cancer occurrence and progression. However, whether and how RBM39 regulates BER in hepatocellular carcinoma (HCC) remain unclear. Here, we found that under oxidative stress, RBM39 degradation or knockdown decreased BER efficiency in HCC cells using a well-designed BER reporter. Further assays showed that RBM39 promoted HCC cell proliferation, migration, and invasion, enhancing cell survival and inhibiting apoptosis. Mechanistically, RBM39 interacted with the mRNA of the essential glycosidase 8-oxoguanine-DNA glycosylase 1 (OGG1), thereby stabilising OGG1 mRNA. This in turn increases OGG1 expression and promotes BER efficiency in HCC. Moreover, data suggested that RBM39 degradation, combined with oxidative damage, could be more effective for HCC treatment than monotherapy, both in vitro and in xenograft mice models. Overall, we demonstrated that RBM39 regulated OGG1 stabilisation and improved BER efficiency, suggesting that combining the RBM39 degradant indisulam with the oxidising agent KBrO
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