ArticleChinese medical journal2026
Epigenetically elevated RAD51AP1 regulates the RAD51-UAF1 complex contributing to temozolomide resistance in EGFRvIII glioblastoma.
Article in Chinese medical journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- P4HA1 mediates YAP hydroxylation and accelerates collagen synthesis in temozolomide-resistant glioblastoma.Chinese medical journal · 2025Article
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9 authors.
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Abstract
backgroundEpidermal growth factor receptor variant III ( EGFRvIII ) mutation is the most prevalent genetic change in glioblastoma. Abnormal DNA damage repair caused by EGFRvIII, which leads to temozolomide (TMZ) resistance, is a major cause of reduced postoperative survival in glioblastoma patients. This study aims to uncover the molecular mechanism of TMZ resistance in EGFRvIII -mutant glioblastoma.
methodsWe constructed a Clustered regularly interspaced shortpalindromic repeats (CRISPR)/CRISPR-associated (Cas) system 9 library to identify synthetic lethal genes for EGFRvIII -bearing cells. Abnormal epigenetic regulation of the RAD51-associated protein 1 ( RAD51AP1 ) promoter was assessed via chromatin immunoprecipitation sequencing (ChIP-seq) and chromatin immunoprecipitation polymerase chain reaction (ChIP-PCR) analyses. In vitro and in vivo experiments were carried out to investigate the role of the RAD51AP1 gene in TMZ resistance in EGFRvIII -bearing glioblastoma.
resultsThe CRISPR/Cas9 library identified RAD51AP1 , a synthetic lethal gene for EGFRvIII -bearing cells exposed to TMZ. ChIP-seq and ChIP-PCR analyses revealed that acetylated histone H3 lysine 27 (H3K27ac) and SRY-box transcription factor 9 ( SOX9 ) together induced RAD51AP1 transcription in EGFRvIII cells. High expression levels of RAD51AP1 , promoted formation of the RAD51-UAF1 complex to activate homologous recombination and inhibit TMZ-induced DNA damage.
conclusionThe results of this study suggest that aberrant RAD51AP1 expression is a crucial mechanism by which EGFRvIII -mutant glioblastoma resists TMZ chemotherapy, laying the groundwork for future personalized medicine.
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