ArticleTranslational oncology2025
BUB1B promotes cisplatin resistance in gastric cancer via Rad51-mediated DNA damage repair.
Article in Translational oncology, 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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Who cites it
3 citing papers in PubMed.
- BUB1B is a novel prognostic-related biomarker and correlated with immune infiltrates in lung adenocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Unveiling the mechanistic links between plasticizers and gastric cancer via network toxicology and molecular docking approaches.BMC pharmacology & toxicology · 2025Article
- Liver fibrosis in biliary atresia: identification of the key gene EDIL3 via integrated bioinformatics.Frontiers in medicine · 2025Article
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Authors and funding
7 authors.
Funding
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Abstract
backgroundCisplatin resistance significantly impedes the treatment of gastric cancer (GC). This work examined the possible therapeutic target status and function of BUB1B in controlling cisplatin resistance.
methodsFollowing the identification of differentially expressed genes (DEGs), protein-protein interaction (PPI) network analysis was conducted using datasets from the Cancer Genome Atlas-stomach adenocarcinoma (TCGA-STAD), GSE51575, and GSE79973. Functional tests assessed the effect of BUB1B overexpression and knockdown on the GC cells. Enrichment analysis and RNA-seq identified pathways linked to BUB1B. Additionally, the function of BUB1B in GC cells resistant to cisplatin in regulating DNA repair was examined, as its relationship with Rad51 inhibitor (B02) in regulating cell cycle, proliferation, and apoptosis. The combined effects of Rad51 suppression and BUB1B overexpression on tumor development in cisplatin-resistant GC cells were further validated in vivo xenograft models.
resultsSignificant overexpression of six critical overlapping genes was seen in GC tissues. The GC cell invasion, migration, and proliferation processes were improved by BUB1B overexpression, whereas BUB1B knockdown prevented these outcomes. Genes involved in DNA repair were downregulated by BUB1B knockdown, according to an RNA-seq study. BUB1B overexpression boosted cell survival via modulating cell cycle proteins, but BUB1B knockdown hampered DNA repair and increased death in cisplatin-resistant GC cells. Overexpression of BUB1B enhanced tumor development in vivo and counteracted the inhibitory effects of B02 on cell growth.
conclusionBUB1B enhances cisplatin resistance in gastric cancer by regulating DNA repair and cell cycle progression, suggesting that targeting BUB1B may be a feasible therapeutic strategy.
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