Conclusion

This review has highlighted the therapeutic potential of PARP inhibitors in prostate cancer as a monotherapy or in combination with another type therapy. PARP-1 is implicated in stabilizing the genomic content as well as in the selection of cells with unrepaired DNA damaged. A large body of evidence has demonstrated that inhibition of PARP-1 was sufficient to promote the development of tetraploidy in normal cells and effectively enhanced DNA damage in response to genotoxic agents. These results proved that the physical disruption of PARP-1 is essential for the maintenance of genomic instability. The increased expression of PARP-1 in a series of tumors has been related with cell proliferation and determination of the biological behavior of tumors, events that may predict the overall prognosis of the cancer. In this regard, studies on prostate cancer models in vitro and in vivo have shown that PARP inhibitions regulated the growth of tumors or prevented tumor invasion to other organs. Although several studies have provided promising results in treating advanced tumors, few clinical trials are available in prostate cancer, one of the most prevalent cancers affecting men. Indeed, PARP inhibitors are currently tested in breast cancer patients with mutations in the BRCA1 and BRCA2, which are also mutated in a significant number of prostate cancers. Since advanced prostate cancer generally develops resistance to chemo-therapeutic and hormone therapies, the identification of mechanisms underlying prostate cancer progression is vital to identify potential targets for prostate cancer therapy. Recent findings have demonstrated that BRCA1 and BRCA2 mutations confer sensitivity to PARP inhibitors, promoting genomic instability and cell death, and that tumors with BRCA1 mutated are potential targets for a new generation of non-toxic PARP inhibitors. Moreover, the mechanism by which PARP-1 inhibition and BRCA mutations allow the accumulation of DNA errors and the promotion of tumor growth in prostate cells may provide the basis to develop more effective strategies for therapeutic intervention. However, the identification of new genetic markers are necessary to define the feasibility of PARP-1 as a therapeutically target for the treatment of patients with prostate cancer.

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