ArticleJournal of experimental & clinical cancer research : CR2025
USP43 promotes gemcitabine resistance by regulating cholesterol homeostasis through E2F1 stabilization in bladder cancer.
Article in Journal of experimental & clinical cancer research : CR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- DHCR24Oncogene · 2026Article
- Multimodal AI and single-cell transcriptomics integrate to construct a histopathological prognostic model for bladder cancer, revealing the RTN3-glycolysis axis in chemoresistance.Experimental hematology & oncology · 2026Article
- NAT10 promotes gallbladder cancer progression by remodeling cholesterol metabolism via PCSK9 mRNA acetylation.Cell death discovery · 2026Article
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Authors and funding
15 authors.
Funding
Abstract
backgroundGemcitabine (GEM) is a standard treatment for bladder cancer (BLCA), but resistance to this chemotherapy often reduces its efficacy. Thus, to uncover the molecular mechanisms of this resistance is essential to reverse GEM resistance.
methodsTo explore the role of the USP43/E2F1/NSDHL pathway in GEM resistance in BLCA, we employed integrated analytical approaches including gene expression profiling, biochemical assays, xenograft models, among others.
resultsWe discovered that the oncogene E2F1, which is highly expressed in GEM-resistant BLCA cells, plays a significant role in promoting resistance to the drug. We found that E2F1 enhances GEM resistance by activating NSDHL, an enzyme crucial for cholesterol biosynthesis, leading to increased cholesterol levels. We also identified USP43 as the deubiquitinase that stabilizes E2F1, contributing to its increased expression in response to GEM.
conclusionOur study indicates the USP43/E2F1/NSDHL pathway as a key mechanism in cholesterol-mediated GEM resistance in BLCA, providing novel insights for therapeutic intervention to counteract chemoresistance.
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