Our overall hypotheses are that EZH2 represses PARP1 activity by methylating the lysines of PARP1 and acts as a PARP1 co-factor to recruit PARP1 to genomic loci during the DNA damage response in advanced PCa and CRPC. Overexpression of EZH2 and PARP1 will promote PCa progression, and inhibition of both EZH2 and PARP1 will benefit PCa and CRPC patients.
|Effective start/end date||7/1/18 → 8/31/21|
- U.S. Army Medical Research and Materiel Command (W81XWH-17-1-0357 P00001)
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