ArticleCell death & disease2022
Inhibition of USP1 enhances anticancer drugs-induced cancer cell death through downregulation of survivin and miR-216a-5p-mediated upregulation of DR5.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Cathepsin L deletion enhances sensitivity to anticancer drugs through Parkin-mediated ubiquitination of Bcl-xL and USP53-induced Survivin destabilization.Cell death and differentiation · 2026Article
- Article
- Inhibition of UBE2N enhances TRAIL-mediated apoptosis through upregulation of DR5 in cancer cells.International journal of medical sciences · 2026Article
- Biochemical and Comparative Proteomic Analyses Delineate the Anti-Ovarian Carcinogenic Roles of Modified Calycosin.Food science & nutrition · 2026Article
- The USP1-WDR48 deubiquitinase complex functions as a molecular switch regulating tumor-associated macrophage activation and anti-tumor response.Cell death and differentiation · 2026Article
- Circular RNA circMYBL2 regulates the progression of ovarian cancer through miR-195-5P/BIRC5 axis.Journal of ovarian research · 2025Article
- USP1-TRAF2 axis-regulated mortalin stability mediates chemoresistance by disrupting calcium transport in peripheral T-cell lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Survivin Is a Central Mediator of Cell Proliferation in HPV-Negative Head and Neck Squamous Cell Carcinoma.Cancers · 2025Article
- AKT and DUBs: a bidirectional relationship.Cellular & molecular biology letters · 2025Review
- Exosomal transfer of pro-pyroptotic miR-216a-5p exacerbates anthracycline cardiotoxicity through breast cancer-heart pathological crosstalk.Signal transduction and targeted therapy · 2025Article
- SJB2-043, a USP1 Inhibitor, Suppresses A549 Cell Proliferation, Migration, and EMT via Modulation of PI3K/AKT/mTOR, MAPK, and Wnt Signaling Pathways.Current issues in molecular biology · 2025Article
- Ubiquitin-Specific Protease Inhibitors for Cancer Therapy: Recent Advances and Future Prospects.Biomolecules · 2025Review
- Ubiquitin-specific protease 1 facilitates tumor immune escape from natural killer cells and predicts the prognosis in small cell lung cancer.Oncology research · 2025Article
- Article
- Deubiquitinating enzymes: potential regulators of the tumor microenvironment and implications for immune evasion.Cell communication and signaling : CCS · 2024Review
- Deubiquitinase USP1 regulates sarbecovirus ORF6 protein function.Journal of virology · 2024Article
- BIRC5 facilitates cisplatin-chemoresistance in a mCancer medicine · 2024Article
- BIRC5 as a prognostic and diagnostic biomarker in pan-cancer: an integrated analysis of expression, immune subtypes, and functional networks.Frontiers in genetics · 2024Article
- Roles of USP1 in Ewing sarcoma.Genes & cancer · 2024Article
- Polymorphisms in miRNA Genes Targeting the AMPK Signaling Pathway are Associated with Cervical Cancer Susceptibility in a Han Chinese Population.International journal of general medicine · 2024Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ubiquitin-specific protease 1 (USP1) is a deubiquitinase involved in DNA damage repair by modulating the ubiquitination of major regulators, such as PCNA and FANCD2. Because USP1 is highly expressed in many cancers, dysregulation of USP1 contributes to cancer therapy. However, the role of USP1 and the mechanisms underlying chemotherapy remain unclear. In this study, we found high USP1 expression in tumor tissues and that it correlated with poor prognosis in RCC. Mechanistically, USP1 enhanced survivin stabilization by removing ubiquitin. Pharmacological inhibitors (ML23 and pimozide) and siRNA targeting USP1 induced downregulation of survivin expression. In addition, ML323 upregulated DR5 expression by decreasing miR-216a-5p expression at the post-transcriptional level, and miR-216a-5p mimics suppressed the upregulation of DR5 by ML323. Inhibition of USP1 sensitized cancer cells. Overexpression of survivin or knockdown of DR5 markedly prevented the co-treatment with ML323 and TRAIL-induced apoptosis. These results of in vitro were proved in a mouse xenograft model, in which combined treatment significantly reduced tumor size and induced survivin downregulation and DR5 upregulation. Furthermore, USP1 and survivin protein expression showed a positive correlation, whereas miR-216a-5p and DR5 were inversely correlated in RCC tumor tissues. Taken together, our results suggest two target substrates of USP1 and demonstrate the involvement of survivin and DR5 in USP1-targeted chemotherapy.
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