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. 2011 Apr 29;6(4):e19103. doi: 10.1371/journal.pone.0019103

Figure 2. vGPCR secretions regulate TSC/mTOR through multiple signaling pathways in vitro and in vivo.

Figure 2

(A) HMEC1s were pretreated with vehicle or inhibitors of the AKT, ERK, p38 or IKKβ pathways, LY294002 (50 µM), U0126 (50 µM), SB203580 (50 µM) or BAY11-7082 (40 µM). Cells were then exposed to media conditioned by control cells (Control CM) or vGPCR-expressing cells (vGPCR CM). Phosphorylation levels of the corresponding kinase (AKT, ERK1/2, p38 or IKKβ), TSC2/1 targeted phosphorylation site (P-TSC2T1462, P-TSC2S664, P-TSC2S1254 or P-TSC1S511), and S6K are shown. (B) HMEC1s were transfected with Scrambled siRNA or siRNA for AKT, ERK (ERK1 and 2), p38 or IKKβ. Cells were then exposed to media conditioned by control or vGPCR-expressing cells. Levels of the corresponding kinase (AKT, ERK1/2, p38 or IKKβ) and S6K are shown. (C) Immunohistochemical staining of vGPCR tumors and human KS with antibodies against P-AKT, P-ERK, P-p38 or P-IKKβ, and the corresponding TSC2/1 targeted phosphorylation site, P-TSC2T1462, P-TSC2S664, P-TSC2S1254 or P-TSC1S511.