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. Author manuscript; available in PMC: 2009 Oct 14.
Published in final edited form as: Cancer Biol Ther. 2009 Jul 30;8(14):1389–1401. doi: 10.4161/cbt.8.14.8880

Figure 6. Akt regulates YY1 protein expression.

Figure 6

A. The 786-0 cells were treated with either vehicle (DMSO) alone, the PI3K inihibitor, LY294002 [10μM], the Akt inhibitor, triciribine [20μM, 40μM], or the mTOR inhibitor, rapamycin [20nM] in serum-free conditions overnight. Whole cell lysates were purified and immunoblotted for P-Akt (ser473), YY1, and HIF-2α. Actin was used as a loading control. B. The 786-0 cells were transfected with 50nM of control siRNA or siRNAs specifically targeting both Akt1 and Akt2 isoforms. Whole cell lysates were harvested 24 hrs later and immunoblotted for total Akt, YY1, HIF-2α and actin as a loading control. The 786-0 cells were co-transfected with the HRE-luc and either treated with 20μM triciribine (C) or co-transfected with 50nM of control or Akt1, 2 siRNAs (D). Transfectants were harvested after 24 hrs and analyzed for luciferase activity. Results represent three independent experiments of triplicate samples. Columns, mean; bars, SD; p<0.0001 (***). E. 786-0 cells were transfected with 50nM of control or Akt2 specific siRNAs for 24hrs. Whole cells lysates were then purified and analyzed by immunoblotting for total Akt2, YY1, HIF-2α, and actin as a loading control.