The WRN protein along with ATM, BRCA1, BRCA2, and RAD51 among others, comprise a DNA repair system by homologous recombination, and its alterations are associated with forms of hereditary PCa.
Pharmacologic Stat5a/b inhibition potently sensitized prostate cancer cell lines and prostate cancer tumors to radiation, while not inducing radiation sensitivity in the neighboring tissues.<b>Conclusions:</b> This work introduces a novel concept of a pivotal role of Jak2-Stat5a/b signaling for Rad51 expression and HR DNA repair in prostate cancer.
No association was observed between PTEN-status and RAD51 expression either in-vitro or in-vivo in a tissue microarray of 1500 PTEN-deficient prostate cancer (PC) samples.
Accumulation of endogenous p53 but not E2F1 and suppressed RAD51 transcription was observed in prostate cancer line with wild-type p53 after DNA damage under hypoxia.
Decreased PTEN expression did not reduce RAD51 expression or clonogenic survival following PARPi among prostate cancer cells that vary in TP53 and PTEN.
We examined the association between PC risk with nonsynonymous SNPs (nsSNPs) in 5 genes involved in 3 DNA-repair pathways: (1) base excision repair (BER): hOGG1 C1245G (Ser326Cys) and XRCC1 G28152A (Arg399Gln); (2) nucleotide excision repair (NER): XPD G23591A (Asp312Asn); (3) homologous recombination repair: RAD51G135C (in 5' untranslated region) and XRCC3 C18067T (Thr241Met).