The Oncogenic Role of WWP1 E3 Ubiquitin Ligase in Prostate Cancer Development

2011 ◽  
Author(s):  
Ceshi Chen
Keyword(s):  
Prostate Cancer ◽  
Ubiquitin Ligase ◽  
E3 Ubiquitin Ligase ◽  
Cancer Development ◽  
Prostate Cancer Development

Abstract 1862: Discerning the role of USP22 in prostate cancer development and progression

2015 ◽  
Author(s):  
Jennifer Jones ◽  
Jeffry L. Dean ◽  
Randy S. Schrecengost ◽  
Karen Knudsen
Keyword(s):  
Prostate Cancer ◽  
Cancer Development ◽  
Prostate Cancer Development

scholarly journals G3BP1 inhibits Cul3SPOP to amplify AR signaling and promote prostate cancer

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Chandrani Mukhopadhyay ◽  
Chenyi Yang ◽  
Limei Xu ◽  
Deli Liu ◽  
Yu Wang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Targeted Therapy ◽  
Ubiquitin Ligase ◽  
E3 Ubiquitin Ligase ◽  
Competitive Inhibitor ◽  
Functional Studies ◽  
Specific Tumor ◽  
Signaling Axis ◽  
Oncogenic Function

AbstractSPOP, an E3 ubiquitin ligase, acts as a prostate-specific tumor suppressor with several key substrates mediating oncogenic function. However, the mechanisms underlying SPOP regulation are largely unknown. Here, we have identified G3BP1 as an interactor of SPOP and functions as a competitive inhibitor of Cul3SPOP, suggesting a distinctive mode of Cul3SPOP inactivation in prostate cancer (PCa). Transcriptomic analysis and functional studies reveal a G3BP1-SPOP ubiquitin signaling axis that promotes PCa progression through activating AR signaling. Moreover, AR directly upregulates G3BP1 transcription to further amplify G3BP1-SPOP signaling in a feed-forward manner. Our study supports a fundamental role of G3BP1 in disabling the tumor suppressive Cul3SPOP, thus defining a PCa cohort independent of SPOP mutation. Therefore, there are significantly more PCa that are defective for SPOP ubiquitin ligase than previously appreciated, and these G3BP1high PCa are more susceptible to AR-targeted therapy.

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