Figure 9 | Scientific Reports

Figure 9

From: In vitro and in vivo study of epigallocatechin-3-gallate-induced apoptosis in aerobic glycolytic hepatocellular carcinoma cells involving inhibition of phosphofructokinase activity

Figure 9

Mode of EGCG-induced apoptosis in HCC cells.

Glucose uptake by GLUT2 and aerobic glycolysis by PFK are inhibited with EGCG, resulting in the suppression of ATP production. This leads to mitochondrial membrane potential breakdown and causes direct caspase-8 activation, resulting in caspase-3 activation and cell death. The interaction of EGCG and PFK frees Bad, which interacts with the anti-apoptotic Bcl-2 family proteins Bcl-2 and Bcl-xl to relieve their inhibition of pro-apoptotic proteins Bax and Bak. Oligomerization and activation of Bax and Bak leads to mitochondrial outer membrane permeabilization. Permeabilization of the mitochondrial membranes leads to the release of cytochrome c into the cytoplasm and activation of caspase-9 and caspase-3, resulting in nuclear DNA fragmentation and cell apoptosis.

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