Fig. 6: Graphical scheme.

Schematic representation of the G9a-p53-Bcl-G circuit that controls liver tumor initiation from DNA-damaged hepatocytes. DEN-exposed pericentral hepatocytes undergo DNA damage and mutagenesis. G9a allows DNA-damaged hepatocytes to escape p53-induced apoptosis, the potent genome surveillance checkpoint, via Bcl-G silencing, which results in the fixation of mutations and promotion of future HCC development. In summary, G9a determines whether hepatocytes undergo apoptosis or survive during DNA damage response via the regulation of p53 transactivation.