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. 2017 Mar 31;8(20):33316–33328. doi: 10.18632/oncotarget.16741

Figure 5. Pharmacologic activation of the p38 pathway leads to decreased EGFR and poor self-renewal capacity of the GSC.

Figure 5

(A) GSC treated with anisomycin, a p38 activator, were evaluated by Western blotting. Anisomycin enhances the phosphorylation state of p38 in a dose-dependent manner. (B) Untreated control (solid gray) and GSC exposed to anisomycin (10 μM) for 1 hour were analyzed for expression of EGFR by FACS (left). The reduced expression of EGFR seen with anisomycin treatment was abrogated with addition of SB203580 (10 mM). (C) The reversal of EGFR expression upon p38 inhibition by SB203580 on GSC treated with anisomycin was observed in all lines studied. Data from three representative lines are shown. The results shown in the graph are mean ± S.D. from three experiments. *p < 0.05. (D) The in vitro self-renewal capacity of untreated control and GSC exposed to anisomycin (3 μM for 48 hours) was assessed by sphere-forming assay. Activation of the p38 pathway led to striking reduction of self-renewal. The results shown in the graph are mean + S.D. from three experiments. *p < 0.05.