Anticancer Properties of PPAR-Effects on Cellular Metabolism and Inflammation
Figure 2
PPARα and AMPK activities in the cancer cells exposed to
energetic stress. AMPK switches on p53-dependent cell cycle metabolic check
point and autophagy and blocks Akt/mTOR protein de novo synthesis pathway.
PPARα induces cell cycle arrest and
downregulates Akt neutralizing its antiapoptotic actions. For more details, see
the text. Arrowheads represent activation/upregulation, and blunted lines
indicate inhibition/downregulation of the cellular proteins or processes.
IRS-1—insulin receptor substrate-1; mTOR—mammalian target of rpamycin kinase; TSC1—tuberous sclerosis 1 (hamartin); TSC2—tuberous sclerosis 2 (tuberin).
