ArticleBMC urology2024
USP54 is a potential therapeutic target in castration-resistant prostate cancer.
Article in BMC urology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- USP54 Promotes Ferroptosis in Non-Small Cell Lung Cancer by Mediating FOXA2 Deubiquitination and Enhancing ACSL4 Transcription.The Kaohsiung journal of medical sciences · 2026Article
- Machine learning-based determination of sex-related bladder cancer biomarkers.Frontiers in bioinformatics · 2026Article
- Machine-learning-based determination of sex-related bladder cancer biomarkers.bioRxiv : the preprint server for biology · 2025Article
- Elevated VRK1 levels after androgen deprivation therapy promote prostate cancer progression by upregulating YAP1 expression.Journal of cancer research and clinical oncology · 2025Article
- Targeting USP42 induces DNA damage and inhibits cell growth in prostate cancer.Frontiers in molecular biosciences · 2025Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundUSP54, a ubiquitin-specific protease in the deubiquitinase (DUB) family, facilitates the malignant progression of several types of cancer. However, the role of USP54 in prostate cancer (PCa), especially castration-resistant prostate cancer (CRPC), remains unknown.
methodsWe established the CRPC LNCaP-AI cell line from the hormone-sensitive prostate cancer (HSPC) LNCaP cell line. RNA-Seq was utilized to explore DUB expression levels in LNCaP and LNCaP-AI. USP54 was knocked down, and its effects on cell growth were evaluated in vitro and in vivo. Bioinformatics analyses were conducted to explore signaling pathways affected by USP54 in PCa. Quantitative polymerase chain reaction was used to confirm key signaling pathways involved.
resultsUSP54 was the most strongly upregulated DUB in LNCaP-AI cells compared with LNCaP cells. USP54 levels were higher in PCa than in normal tissues. USP54 silencing suppressed the proliferation of PCa cell lines, both in vitro and in vivo. USP54 expression was positively correlated with the androgen receptor (AR) signaling level in PCa samples, and USP54 knockdown inhibited AR signaling in PCa cells.
conclusionsUSP54 was upregulated during HSPC progression to CRPC. USP54 depletion suppressed CRPC cell proliferation both in vitro and in vivo. USP54 may facilitate PCa progression by regulating AR signaling.
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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.