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. Author manuscript; available in PMC: 2009 Jun 15.
Published in final edited form as: Biochim Biophys Acta. 2006 Oct 7;1773(8):1263–1284. doi: 10.1016/j.bbamcr.2006.10.001

Figure 4. Interactions between Raf/MEK/ERK and Apoptotic Pathways Resulting in Drug Resistance.

Figure 4

Some of the potential downstream molecules activated by the Raf/MEK/ERK, PI3K/Akt and p53 and their effects on the induction of apoptosis are illustrated. The effects of Raf/MEK/ERK and PI3K/Akt on phosphorylation of apoptotic regulatory molecules which exert their effects on mitochondrial membrane potential and the prevention of apoptosis are indicated. Phosphorylation of these molecules by Raf/MEK/ERK and PI3K/Akt is associated with prevention of the caspase cascade and the induction of apoptosis. Activation of p53 by genotoxic stresses can result in the activation of PUMA and NOXA which can have pro-apoptotic effects. Activation of p53 can also result in transcription of hbEGF which would be predicted to have growth stimulatory effects. Drug resistance can result from Raf/MEK/ERK and PI3K/Akt pathways disrupting the balance between induction and prevention of apoptosis.