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. 2023 Sep 19;33(11):835–850. doi: 10.1038/s41422-023-00874-4

Fig. 7. PHGDH modulates HCC growth through p53.

Fig. 7

a, b Liver-specific knockout of Trp53 abolishes the effects of PHGDH on apoptosis and HCC development. The MYC;Trp53−/− HCC mouse models with liver-specific expression of PHGDH mutants were established (a). Statistics of tumor numbers were determined and are shown in b (determined as in Fig. 5d; data are means ± SD, n  =  6–8 (left) or 6–7 (right), with P values calculated by one-way (left) or two-way (right) ANOVA, followed by Tukey). See also apoptotic markers of liver tissues from HCC mice in Supplementary information, Fig. S7a. c A schematic diagram depicting that PHGDH senses low 3-PGA to induce apoptosis in the control of cell fate. In low glucose, increased portion of PHGDH becomes unoccupied with 3-PGA, and displays a stronger affinity towards AXIN. As a result, TIP60 is recruited to AXIN, which helps dissociate PIRH2 from and promotes HIPK2 binding to AXIN. This leads to the formation of the AXIN–TIP60–HIPK2–p53 complex, where HIPK2 phosphorylates Ser46 of and activates p53 to induce apoptosis. Experiments were performed three times.