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ABSTRACT: Background
The deregulated expression of the c-MYC oncogene activates p53, which is presumably mediated by ARF/INK4, as well as replication-stress-induced DNA damage. Here, we aimed to determine whether the c-MYC-inducible AP4 transcription factor plays a role in this context using a genetic approach.Methods
We used a CRISPR/Cas9 approach to generate AP4- and/or p53-deficient derivatives of MCF-7 breast cancer cells harboring an ectopic, inducible c-MYC allele. Cell proliferation, senescence, DNA damage, and comprehensive RNA expression profiles were determined after activation of c-MYC. In addition, we analyzed the expression data from primary breast cancer samples.Results
Loss of AP4 resulted in elevated levels of both spontaneous and c-MYC-in
SUBMITTER: Kaller M
PROVIDER: S-EPMC9954515 | biostudies-literature | 2023 Feb
REPOSITORIES: biostudies-literature