The function of MYC in base excision repair protects against RAS-induced senescence.
Ontology highlight
ABSTRACT: The MYC and RAS oncogenes were found early on to cooperate in the transformation of nonimmortalized primary cells, and in tumor development in transgenic mouse models. MYC prevents RAS-induced senescence. Moreover, tumor regression resulting from the suppression of MYC expression is associated with cellular senescence. How MYC prevents RAS-induced senescence and why suppression of MYC in tumors causes senescence remains to be elucidated. Here, we show that MYC interacts with the Pol β DNA polymerase and stimulates its enzymatic activities to accelerate the repair of oxidative DNA damage by the base excision repair (BER) pathway, thereby enabling RAS-driven cancer cells to avoid senescence and continue to proliferate despite producing excess levels of reactive oxygen species. The carboxy-te
SUBMITTER: Faraco CCF
PROVIDER: S-EPMC12309371 | biostudies-literature | 2025 Jul
REPOSITORIES: biostudies-literature
ACCESS DATA