Alternative Non-Homologous End-Joining: Error-Prone DNA Repair as Cancer's Achilles' Heel.

ABSTRACT: Error-prone DNA repair pathways promote genomic instability which leads to the onset of cancer hallmarks by progressive genetic aberrations in tumor cells. The molecular mechanisms which foster this process remain mostly undefined, and breakthrough advancements are eagerly awaited. In this context, the alternative non-homologous end joining (Alt-NHEJ) pathway is considered a leading actor. Indeed, there is experimental evidence that up-regulation of major Alt-NHEJ components, such as LIG3, PolQ, and PARP1, occurs in different tumors, where they are often associated with disease progression and drug resistance. Moreover, the Alt-NHEJ addiction of cancer cells provides a promising target to be exploited by synthetic lethality approaches for the use of DNA damage response (DDR) inhibitors and

SUBMITTER: Caracciolo D 

PROVIDER: S-EPMC8003480 | biostudies-literature | 2021 Mar

REPOSITORIES: biostudies-literature