Pharmacological methods to transcriptionally modulate double-strand break DNA repair.

ABSTRACT: There is much interest in targeting DNA repair pathways for use in cancer therapy, as the effectiveness of many therapeutic agents relies on their ability to cause damage to DNA, and deficiencies in DSB repair pathways can make cells more sensitive to specific cancer therapies. For example, defects in the double-strand break (DSB) pathways, non-homologous end joining (NHEJ) and homology-directed repair (HDR), induce sensitivity to radiation therapy and poly(ADP)-ribose polymerase (PARP) inhibitors, respectively. However, traditional approaches to inhibit DNA repair through small molecule inhibitors have often been limited by toxicity and poor bioavailability. This review identifies several pharmacologic manipulations that modulate DSB repair by reducing expression of DNA repair factors. A

SUBMITTER: Kaplan AR 

PROVIDER: S-EPMC7577782 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature