ArticleCell death discovery2022
Deubiquitinase USP35 stabilizes BRPF1 to activate mevalonate (MVA) metabolism during prostate tumorigenesis.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Mechanism of lovastatin in promoting ferroptosis of prostate cancer cells by regulating the mevalonate pathway.European journal of histochemistry : EJH · 2026Article
- Atorvastatin as a pleiotropic anticancer agent: mechanisms, evidence, and therapeutic repurposing potential.Frontiers in immunology · 2026Review
- The deubiquitinase USP35: from an oncogenic hub to a therapeutic target in human cancers.Frontiers in oncology · 2026Review
- BRPF1 in cancer epigenetics: a key regulator of histone acetylation and a promising therapeutic target.Cell death discovery · 2025Review
- BRPF1 inhibition reduces migration and invasion of metastatic ovarian cancer cells, representing a potential therapeutic target.Scientific reports · 2025Article
- SREBP2 as a central player in cancer progression: potential for targeted therapeutics.Frontiers in pharmacology · 2025Review
- The role of ubiquitination and deubiquitination in cancer lipid metabolism.Frontiers in oncology · 2025Review
- Overexpression of USP35 enhances the protective effect of hUC-MSCs and their extracellular vesicles in oxygen-glucose deprivation/reperfusion-induced SH-SY5Y cells via stabilizing FUNDC1.Communications biology · 2024Article
- Exploiting epigenetic targets to overcome taxane resistance in prostate cancer.Cell death & disease · 2024Article
- Ubiquitin-specific Protease 35 Promotes Gastric Cancer Metastasis by Increasing the Stability of Snail1.International journal of biological sciences · 2024Article
- USP35 promotes HCC development by stabilizing ABHD17C and activating the PI3K/AKT signaling pathway.Cell death discovery · 2023Article
- Bromodomain (BrD) Family Members as Regulators of Cancer Stemness-A Comprehensive Review.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mutual interplay between epigenetic modifications and metabolic rewiring contributes to malignant features of prostate adenocarcinoma (PRAD). This study aimed to uncover the biological roles of deubiquitylase USP35 in PRAD and find effective epigenetic or metabolic targets. Bioinformatic tools or methods revealed that USP35 is upregulated in PRAD samples and correlates with inferior prognosis. The in vitro and in vivo assays suggested that USP35 could enhance malignant features of PRAD cells. Mechanistically, we found that USP35 could directly deubiquitinate and stabilize BRPF1 proteins. USP35 depends on accumulated BRPF1 proteins to accelerate cell growth, stem-like properties, and migration in vitro and in vivo. Interestingly, high BRPF1 could bind to promoter of SREBP2 and activate the SREBP2 transcriptional capacity. Therefore, USP35/BRPF1 aixs could promote expressions of mevalonate (MVA) metabolism signature in a SREBP2-dependent manner. USP35 depends on BRPF1 to maintain the activity of mevalonate metabolism in PRAD cells. Last of all, we observed that targeting BRPF1 or using MVA inhibitor (atorvastatin) are effective to suppress USP35
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.