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Updated: Jun 19, 2025
11:29
miRNA Expression Analyses in Prostate Cancer Clinical Tissues
Published on: September 8, 2015
10.8K
USP11 promotes prostate cancer progression by up-regulating AR and c-Myc activity
Majid Pornour1,2, Hee-Young Jeon1,2, Hyunju Ryu1,2
1Department of Biochemistry and Molecular Biology, University of Maryland, Baltimore, MD 21201.
Summary
The deubiquitinase USP11 promotes aggressive prostate cancer (PCa) by stabilizing androgen receptor (AR) and c-Myc. Inhibiting USP11 reduces tumor growth, suggesting it as a therapeutic target for advanced PCa.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Androgen receptor (AR) drives castration-resistant prostate cancer (CRPC).
- The oncogene c-Myc is implicated in prostate tumorigenesis.
- USP11 deubiquitinase activity is increasingly recognized in cancer progression.
Purpose of the Study:
- To investigate the role of USP11 in prostate cancer (PCa) progression.
- To determine if USP11 targets AR and c-Myc in PCa.
- To explore USP11 as a potential therapeutic target for aggressive PCa.
Main Methods:
- USP11 expression analysis in metastatic PCa and CRPC tissues.
- USP11 knockdown (KD) in PCa cells followed by cell growth assays.
- RNA-sequencing and ChIP-sequencing to analyze transcriptional changes and protein binding.
- Assessing the impact of USP11 KD on AR and c-Myc protein stability and gene transcription.
Main Results:
- USP11 expression is elevated in metastatic PCa and CRPC.
- USP11 knockdown significantly inhibits PCa cell proliferation.
- USP11 KD alters AR and c-Myc expression and reduces their binding to chromatin.
- USP11 stabilizes AR and c-Myc proteins and promotes their gene transcription via H2A-K119Ub deubiquitination.
Conclusions:
- USP11 promotes aggressive PCa by upregulating AR and c-Myc stability and transcription.
- USP11 plays a tumor-promoting role in advanced prostate cancer.
- USP11 is a potential therapeutic target for treating PCa.
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