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. 2014 Mar 26;5(9):2372–2389. doi: 10.18632/oncotarget.1706

Figure 3. NVP-AUY922 and NVP-BEZ235 functioned together to block the PI3K/Akt/mTOR signaling pathway.

Figure 3

(A) Western blot analysis revealed the molecular signature of PI3K/mTOR inhibition induced by NVP-AUY922 in the CCA and HuCCT1 cell lines. Cell lysates from the CGCCA and HuCCT1 cell lines were treated with 0.5 uM NVP-AUY922 at various time points (0, 24, 48, 72 h); (B) Western blot analysis reveals the molecular signature induced by NVP-BEZ235 in CCA and HuCCT1 cell lines. Cell lysates from CGCCA and HuCCT1 cells were treated with 0.5 uM NVP-BEZ235 for various time points (0, 24, 48, and 72 h); (C) Western blot analysis revealed the molecular signature induced by NVP-BEZ235 and NVP-AUY922 treatment in CCA and HuCCT1 cell lines. Cell lysates from CGCCA and HuCCT1 cells were treated with 0.5 uM NVP-AUY922 and NVP-BEZ235 at various time points (0, 24, 48, and 72 h). β-Actin was used as the loading control.