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. Author manuscript; available in PMC: 2009 Oct 15.
Published in final edited form as: Cancer Res. 2008 Oct 15;68(20):8361–8368. doi: 10.1158/0008-5472.CAN-08-0878

Figure 2. Treatment of KSHV vGPCR-expressing endothelial cells with PI-103 independently inhibits both PI3K/Akt and mTOR.

Figure 2

(A) Immunodetection of the levels of P-Akt, Akt, P-S6K, S6K, P-S6, S6, P-p38 or p38 of EC-vGPCR cells treated with increasing doses of PI-103 or DMSO (control) for 6 hours. (B) Immunodetection of the levels of P-Akt, Akt, P-S6 or S6 in cells expressing vGPCR or vGPCR and Rheb. Cells were treated with LY294002 (LY), rapamycin (Rap), PI-103 or DMSO (control) for 6 hours. Co-expression of vGPCR with Rheb partially rescued the inhibition of mTOR by LY294002, but not by PI-103 (or rapamycin). (C) Immunodetection of the levels of P-Akt, Akt, P-GSK3, GSK3, P-BAD BAD, P-Mdm2, Mdm2, P-p27 or p27 of EC-vGPCR cells treated with increasing doses of PI-103 or DMSO (control) for 6 hours.

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