Figure 4.

HPyVs’ small tumor antigen (sT-Ag) oncogenic mechanisms. (A) In physiological conditions, the Akt, p53, c-Myc, and β-catenin proteins are in a phosphorylated state; the subsequent dephosphorylation due to the PP2A serine-threonine phosphatase regulates the cell cycle progression and the apoptosis process. (B) The binding between sT-Ag and PP2A avoids the dephosphorylation of Akt, p53, c-Myc, and β-catenin proteins, and the subsequent deregulation of the cell cycle progression and apoptosis process drives the cell to a malignant transformation. HPyVs indicate human polyomaviruses; PP2A, phosphatase 2A.