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. 2016 Sep 29;6:33146. doi: 10.1038/srep33146

Figure 8. Blockage of IGF/IGF-1R signaling prevents BA145 mediated Akt activation and enhances BA145 induced autophagy.

Figure 8

PANC-1 cells were pretreated with specific IGF-1R inhibitor L000391906 (4 μM) for 1 h and then cotreated with BA145 (40 μM) for 3 h. The cells were lysed in lysis buffer and then subjected to western blot analysis of indicated proteins (b) Blockage of IGF-1R signaling with L000391906 prevents BA145 mediated membrane translocation of p-Akt. Cells were treated L000391906 (4 μM) for 1 h and then cotreated with BA145 (40 μM) for 3 h. Cells were stained with immunofluorescent p-Akt (Serine 473) antibody and analyzed by fluorescence microscopy (c) BA145 induces Akt activation in IGF dependent manner. PANC-1 cells were serum starved overnight and cotreated with either BA145 (40 μM) or wortmanin (1 μM) in presence or absence of IGF activator, insulin (100 ng/ml) for 3 h. Cells were lysed in lysis buffer for western blot analysis of Akt, S6K and their phosphorylated forms. β-actin was used as a loading control (d) Effect of L000391906 (4 μM) on the colony forming ability of BA145 (40 μM, 12 h) treated PANC-1 cells (e) Inhibition of IGFR-1 signaling enhanced BA145 mediated autophagy in PANC-1 cells. Cells were treated with BA145 (40 μM) and/or L000391906 (4 μM) for 6 h and then after stained with fluorescent antibody and analyzed by immunofluorescent microscopy. Columns, mean; bars, SD with ***p < 0.001 versus BA145.