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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).