ArticleCell death & disease2024
USP3 promotes DNA damage response and chemotherapy resistance through stabilizing and deubiquitinating SMARCA5 in prostate cancer.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Oncogenic USP3 promotes hepatocellular carcinoma progression via K11/K48-specific deubiquitination and stabilization of YAP.iScience · 2026Article
- ATP-dependent chromatin remodelers in prostate cancer progression and therapeutic resistance.Endocrinology · 2026Review
- Dysregulation of circ-SMARCA5, circ-RHOT1, and HNF1A and the association of HNF1A polymorphisms with hepatocellular carcinoma.Molecular biology reports · 2026Article
- Gut microbiota and its metabolites: Key factors of drug resistance in the treatment of advanced prostate cancer (Review).Molecular medicine reports · 2026Review
- USP10 deubiquitinase: Physiological function, diseases and therapeutic target (Review).International journal of molecular medicine · 2026Review
- Mechanism of RBM15 in the Immune Escape of Non-small Cell Lung Cancer Cells Via the LncRNA EGFR-AS1/USP3/PD-L1 Axis.Biological procedures online · 2026Article
- USP3 stabilizes MIC19 by deubiquitination under hypoxic stress and promotes the progression of non-small cell lung cancer.Acta pharmacologica Sinica · 2026Article
- PIGL promotes the docetaxel resistance of prostate cancer and is regulated by E3 ubiquitin ligase HUWE1.Frontiers in immunology · 2026Article
- OTUB2/ALYREF axis modulates the docetaxel resistance of castration-resistant prostate cancer via upregulating ABCG4-mediated drug efflux.International journal of biological sciences · 2026Article
- Exploring targeted therapies against RFPL3 for non-small cell lung cancer with lymph node metastasis.Discover oncology · 2025Article
- Cisplatin-mediated activation of NF-κB promotes lung cancer stem cell formation via DNA repair pathways.Journal of translational medicine · 2025Article
- The emerging role of E3 ubiquitin ligases and deubiquitinases in metabolic dysfunction-associated steatotic liver disease.Journal of translational medicine · 2025Review
- USP10/XAB2/ANXA2 axis promotes DNA damage repair to enhance chemoresistance to oxaliplatin in colorectal cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Targeting USP42 induces DNA damage and inhibits cell growth in prostate cancer.Frontiers in molecular biosciences · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
The chromatin-remodeling enzyme SMARCA5 plays a key role in DNA-templated events including transcription, DNA replication, and DNA repair. Loss of function of the SMARCA5 can cause neurodevelopmental disorder and Williams syndrome. However, the molecular mechanism underlying the regulation of SMARCA5 in prostate cancer remains largely elusive. Here, we report that the deubiquitinating enzyme USP3 directly interacts with SMARCA5 and removes K63-linked polyubiquitination of SMARCA5 to maintain its stability, which promotes DNA damage repair and chemotherapy resistance. Depletion of USP3 or SMARCA5 promoted PCa cells sensitive to docetaxel and overexpression of USP3 restored the cells resistance to docetaxel treatment in SMARCA5 silenced cells in vitro and vivo. Clinically, USP3 was significantly up-regulated in prostate cancer tissues and positively associated with SMARCA5 expression. Collectively, our findings uncover a novel molecular mechanism for the USP3-SMARCA5 axis in regulating DSB repair with an important role in chemotherapy response in human prostate cancers, highlighting that targeting USP3-SMARCA5 axis could be a valuable strategy to treat USP3/SMARCA5-overexpressing chemotherapy-resistant patients and improve drug treatment.
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