Figure 3.

Summary of apolipoprotein B mRNA editing enzyme catalytic polypeptide‐like (APOBEC)3B transcriptional regulations in cancer cells. APOBEC3B is the main source of mutagenesis in multiple types of cancer. High expression of APOBEC3B and elevated activity have been reported in HER2+ breast cancer, human papillomavirus (HPV)+ cervical cancer, and head and neck squamous carcinoma. Nuclear factor kappa B (NF‐κB) pathway activation,53 DNA replication stress54 and HPV E6/7 oncoproteins and mutant p5352 are able to turn on APOBEC3B expression. In contrast, WT p53 activation suppresses APOBEC3B expression through p21‐mediated transcriptional suppressive complexes occupancy of promoter region of APOBEC3B.51, 52 AID, activation‐induced deaminase; IFN, interferon; TNF, tumor necrosis factor