Figure 5. Involvement of p-Akt pathway in the modulation of PDCD4.

Elevated PTEN and suppressed p-Akt were found in the PDCD4 over-expressing stable clones. When cells were starved with serum-free medium, PDCD4 was un-phosphorylated due to suppressed p-Akt expression. Un-phosphorylated PDCD4 was not recognized by proteasome thus leading to the accumulation of PDCD4. When serum was re-administrated to the cells, up-regulated p-Akt phosphorylated PDCD4, which was then depleted through proteasome degradation. The administration of either PI3K inhibitor LY294002, capable of preventing PDCD4 from being phosphorylated by p-Akt, or proteasome inhibitor MG132, preventing the depletion of PDCD4, leading to the accumulation of PDCD4.