AID/APOBEC proteins edit single-stranded DNA and RNA by cytidine deamination and play a key role in many physiological and pathological processes. They cause cytidine to thymidine or guanidine mutations. APOBEC3 proteins provide defence against viral infections, whereas AID is responsible for antibody diversification. Dysregulation of their expression and activity can lead to off-target mutations throughout the genome and cancer development. APOBEC3A and APOBEC3B are the main cause of mutations in more than half of all tumours. Overexpression of APOBEC3 proteins in the tumour microenvironment can affect the immune response. Recently, AID/APOBEC deaminases have been shown to participate in DNA demethylation, which regulates gene expression. AID/APOBEC proteins could be utilised as targets in cancer treatment and have the potential as prognostic biomarkers for predicting clinical outcomes or as biomarkers for predicting targeted cancer therapies and treatment resistance.
|
