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. Author manuscript; available in PMC: 2011 Jul 27.
Published in final edited form as: Oncogene. 2010 Sep 20;30(4):457–470. doi: 10.1038/onc.2010.421

FIGURE 2. AKT1 is constitutively and inducibly activated in STS cells; its inhibition abrogates migration and invasion.

FIGURE 2

A. STS cell lines and high-grade human STS primary cultures express pAKT (pS473) and all three AKT isoforms to varying levels (WB); B. IP for AKT1, AKT2 and AKT3 and corresponding WB demonstrate that only AKT1 is constitutively phosphorylated in STS cells; C. IP of AKT1, 2, and 3 in STS cells after or without treatment with EGF demonstrates induction of AKT1 and AKT3 phosphorylation but not of AKT2. In contrast, EGF stimulation induces the phosphorylation of AKT2 in MDA231 cells. This differential effect was further demonstrated via an AKT kinase assay using GSK-3 fusion protein as a substrate; D. SKLMS1 cells were transiently transfected with SMARTpool siRNA (20nM; two different pools were used) targeting AKT1 or AKT2; a target-specific knockdown was observed (WB). siRNA Knockdown of AKT1 but not of AKT2 significantly inhibits STS cell migration/invasion (p<0.05). [Graphs represent the average of three repeated experiments ±SEM; * depict statistically significant effects (p<0.05); pAKT WB in all panels refer to pS473] (See also Figure S2)