Fig. 8.

Schematic diagram of the mechanism through which mTOR signalling regulates DNA methylation in HCC. Abnormally activated mTOR increases the phosphorylation of 4E-BP1, enhancing eIF4E release from the 4E-BP1/eIF4E complex. Free eIF4E can bind to the 5′UTR of DNMT1, which contains a PRTE, enhancing the translational efficiency of DNMT1. This process can regulate the DNA methylation profile during carcinogenesis, possibly promoting the development of HCC. Combination treatment with mTOR and epigenetic inhibitors synergistically inhibited HCC