ArticleThoracic cancer2025
USP5-dependent HDAC1 promotes cisplatin resistance and the malignant progression of non-small cell lung cancer by regulating RILP acetylation levels.
Article in Thoracic cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- USP5 in cancer: a therapeutic window into metabolism and drug resistance.Journal of translational medicine · 2026Review
- [Potential Mechanisms and Research Advances of HDAC1 in Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026Review
- Differential transcriptomic modulation by histone deacetylase inhibitor SAHA in LUAD and LUSC.Clinical epigenetics · 2026Article
- Plant-derived exosome-like nanovesicles: dual-function platforms for anticancer therapy and drug delivery.Journal of translational medicine · 2026Review
- Pathological role of deubiquitinating enzymes in lung cancer: recent insights and advances.American journal of cancer research · 2026Review
- Electroacupuncture combined with HDAC1 inhibitor suppress tumor growth via improving the recruitment of intratumor CD8Frontiers in oncology · 2025Article
- USP5-dependent HDAC1 promotes cisplatin resistance and the malignant progression of non-small cell lung cancer by regulating RILP acetylation levels.Thoracic cancer · 2025Article
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Abstract
backgroundNon-small cell lung cancer (NSCLC) is a leading cause of cancer-related deaths worldwide, with cisplatin (DDP) resistance being a significant challenge in its treatment. Histone deacetylase 1 (HDAC1) has been implicated in the regulation of NSCLC progression; however, its role in the resistance of NSCLC to DDP remains unclear.
methodsThe mRNA levels of HDAC1, ubiquitin specific peptidase 5 (USP5), and Rab interacting lysosomal protein (RILP) were analyzed by quantitative real-time polymerase chain reaction. The protein expression of HDAC1, multidrug resistance protein 1 (MRP1) and RILP was detected by western blotting assay or immunohistochemistry assay. The IC
resultsHDAC1 expression was upregulated in DDP-resistant NSCLC tissues and cells. Silencing HDAC1 enhanced the sensitivity of NSCLC cells to DDP, inhibited cell proliferation, invasion, and the formation of microspheres and induced cell apoptosis. USP5 was found to deubiquitinate and stabilize HDAC1 in DDP-resistant NSCLC cells. Moreover, HDAC1 overexpression reversed the effects induced by USP5 silencing. HDAC1 also sensitized Rab-interacting lysosomal protein (RILP) acetylation in DDP-resistant NSCLC cells, and RILP upregulation counteracted the effects of HDAC1 overexpression in DDP-resistant NSCLC cells. HDAC1 silencing also improved the sensitivity of tumors to DDP in vivo.
conclusionUSP5-dependentstabilization of HDAC1 contributed to cisplatin resistance and the malignancy of NSCLC by diminishing the levels of RILP acetylation, which suggested that targeting the HDAC1-USP5axis might represent a novel therapeutic strategy for overcoming DDP resistance in NSCLC patients.
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