Phosphorylation-dependent regulation of SPOP by LIMK2 promotes castration-resistant prostate cancer
Abstract
SPOP, an E3 ubiquitin ligase adaptor, can act either as a tumour suppressor or a tumour promoter. In prostate cancer (PCa), it inhibits tumorigenesis by degrading several oncogenic substrates. SPOP is the most altered gene in PCa (~15%), which renders it ineffective, promoting cancer. The remaining PCa tumours, which retain WT-SPOP, still progress to castration-resistant (CRPC) stage, indicating that other critical mechanisms exist for downregulating SPOP. SPOP is reduced in ~94% of WT-SPOP-bearing prostate tumours; however, no molecular mechanism is known for its downregulation.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Dec 14, 2020
- Source ID
- 10.1038/s41416-020-01197-6
Entities
People
- Hanan S. Haymour
- Kavita Shah
- Kumar Nikhil
- Mohini Kamra
Organizations
- Center for Scientific Review
- Division of Molecular & Cellular Biosciences
- United States Department of Defense