|
| Status |
Public on Sep 26, 2021 |
| Title |
G3BP1 inhibits Cul3SPOP to amplify AR signaling and promote prostate tumorigenesis |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by high throughput sequencing
|
| Summary |
Speckle-type POZ protein (SPOP), an E3 ubiquitin ligase, acts as a tumor suppressor. We identified G3BP1 as non-substrate interactor of SPOP. G3BP1 is a well-known oncogene in many cancer types, but its role in prostate cancer (PCa) remains largely elusive. We showed that G3BP1 functions as an upstream regulator and potent endogenous inhibitor of Cul3SPOP, suggesting a distinctive Cul3SPOP inactivation independent of SPOP mutations. Transcriptomic analysis together with functional studies revealed that the G3BP1-SPOP ubiquitin signaling axis is involved in PCa progression through activating AR signaling. Further, AR upregulates G3BP1 to potentiate feed-forward amplification of signaling through G3BP1-SPOP axis. Overall, we show G3BP1high PCa tumors constitute a new subset where G3BP1 inhibits Cul3SPOP function to upregulate AR signaling, and promotes tumorigenesis.
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| |
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| Overall design |
Differentially expressed genes between loss of G3BP1 vs ctrl and knockdown of SPOP vs ctrl
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| |
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| Contributor(s) |
Mukhopadhyay C, Liu D, Zhou P |
| Citation(s) |
34795264 |
| |
| Submission date |
Oct 08, 2019 |
| Last update date |
Nov 30, 2021 |
| Contact name |
Deli Liu |
| E-mail(s) |
del2017@med.cornell.edu
|
| Organization name |
Weill Cornell Medicine
|
| Street address |
1300 York Ave
|
| City |
New York |
| State/province |
New York |
| ZIP/Postal code |
10021 |
| Country |
USA |
| |
|
| Platforms (1) |
| GPL16791 |
Illumina HiSeq 2500 (Homo sapiens) |
|
| Samples (9)
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|
| Relations |
| BioProject |
PRJNA576506 |
| SRA |
SRP224866 |
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