Analysis of the roles of AP4 and p53 downstream of c-MYC activation in breast cancer cells.

Deregulated expression of the c-MYC oncogene induces unscheduled DNA replication, DNA damage, and activation of the p53 tumor suppressor. The AP4 transcription factor is a direct c-MYC target gene involved in cell proliferation, epithelial-mesenchymal transition, and stemness, as well as suppression of DNA damage and senescence. Here, we analyzed the role of AP4 and p53 downstream of c-MYC activation using a CRISPR/Cas9-approach in MCF-7 cells. Overall design: Cells were pre-treated with ICI for 72 hours. Ectopic expression of c-MYC was induced with DOX for 48 hours in the presence of ICI. For each genotype, RNAs from three biological replicates (48 DOX treatment and ICI-only treated controls) were obtained.