ArticleScience advances2024
VGLL3 modulates chemosensitivity through promoting DNA double-strand break repair.
Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- An antagonistically pleiotropic gene regulates vertebrate growth, maturity, and lifespan.Nature communications · 2026Article
- Global Fibrosis Burden and a Transcriptional Biomarker-Based Strategy for Early Detection in Resource-Limited Settings.Biomolecules · 2025Article
- RNF128 promotes gastric cancer progression by inhibiting autophagy-dependent ferroptosis through Beclin1 ubiquitination.Cell death discovery · 2025Article
- Insights into the DNA damage response and tumor drug resistance.Cancer biology & medicine · 2025Article
- SART3 promotes homologous recombination repair by stimulating DNA-RNA hybrids removal and DNA end resection.Nature communications · 2025Article
- Ubiquitin specific protease 7 is a potential therapeutic target for gastric cancer.Frontiers in oncology · 2025Article
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcription cofactor vestigial-like 3 (VGLL3), as a master regulator of female-biased autoimmunity, also functions in tumor development, while the underlying mechanisms remain largely elusive. Here, we report that VGLL3 plays an important role in DNA damage response (DDR). VGLL3 can be recruited to damage sites in a PARylation-dependent manner. VGLL3 depletion impairs the accumulation of RNF8 and RAD51 at sites of DNA damage, leading to reduced homologous recombination efficiency and increased cellular sensitivity to chemotherapeutic drugs. Mechanistically, VGLL3 can prevent CtIP from KLHL15-mediated ubiquitination and degradation through competitive binding with KLHL15 and, meanwhile, stabilize MDC1 by limiting TRIP12-MDC1 but promoting USP7-MDC1 associations for optimal RNF8 signaling initiation. Consistently, VGLL3 depletion delays tumor development and sensitizes the xenografts to etoposide treatment. Overall, our results reveal an unexpected role of VGLL3 in DDR, which is distinct from its transcriptional cofactor function and not conserved among VGLL family members.
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