Fig. 7
From: aPKC controls endothelial growth by modulating c-Myc via FoxO1 DNA-binding ability
aPKC and miR-34c control angiosarcoma proliferation. a Western blot analysis of c-Myc, pSer218-FoxO1, and total FoxO1 in ISO-HAS-B angiosarcoma cells after treatment with aPKC inhibitor ATG for 24 h. Densitometric quantifications are shown below the lanes mean ±S.E.M.; one-way ANOVA with Bonferroni post-hoc analyses; ***p < 0.001; (n = 3). b Relative BrdU incorporation in ISO-HAS-B cells after treatment with aPKC inhibitors ATG, ATM, or aPKC kinase inhibitor after 24 h. Data represent mean ± S.E.M. two-tailed unpaired t-test **p < 0.01 (n = 6) c Western blot analysis of c-Myc expression in ISO-HAS-B cells after treatment with anti-miR-34c or scrambled control. Densitometric quantifications are shown below the lanes mean + /- S.E.M.; two-tailed unpaired t-test; (n = 3); *p < 0.05. d Relative BrdU incorporation in ISO-HAS-B cells after treatment with anti-miR-34c or scrambled control. Data represent mean ± S.E.M. two-tailed unpaired t-test ****p < 0.0001 (n = 6). e Relative c-Myc expression measured by immunofluorescence in FoxO1-CA or FoxO1-CA/D expressing cells compared to non-transfected neighboring cells; Data represent mean ± S.E.M.; one-way ANOVA with Bonferroni post-hoc analysis; ns p > 0.05 vs. control; *p < 0.05 CA vs. CA/D; ***p < 0.01 vs. control. f Relative EdU incorporation in FoxO1-CA or FoxO1-CA/D expressing cells compared to non-transfected neighboring cells; Data represent mean ± S.E.M. one-way ANOVA with Bonferroni post-hoc analysis; **p < 0.01 CA vs. CA/D; ***p < 0.01 vs. control, ****p < 0.001 vs. control
