Figure 5
Activation of p38MAPK signaling consistently correlates with the FOXC2-dependent EMT/CSC state in androgen-independent PCa cells. Immunoblotting for total (t)- and phospho (p)-p38 and its target substrate ATF2 in PSA+, PSA-/lo cells (a), PCa cell lines (b), LNCaP cells after overexpression of FOXC2 (c) and DU145 cells after suppression of FOXC2 expression (d). (e) Immunoblotting for FOXC2, p- and t-Smad2/3 and p38 signaling components in LNCaP cells induced to undergo EMT using TGFβ1 (a physiological activator of p38 signaling), as well as in DU145 cells treated with LY364947, an inhibitor of TGFβ1 signaling. (f) Quantitation of tumorspheres (n=5; error bars indicate s.e.m.; *P<0.05, ***P<0.001). (g) Schematic shows the putative p38MAPK phosphorylation site on human FOXC2 protein based on phospho-motif scan. (h) Quantitation of tumorspheres (n=5; error bars indicate s.e.m.; **P<0.01, ***P<0.001). (i) Immunoblotting in LNCaP cells expressing the indicated constructs.
