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. 2016 Jun 7;7(29):45060–45078. doi: 10.18632/oncotarget.9911

Figure 6. C3G and p38α MAPK, but not Rap1, promote anchorage dependent growth of HCT116 cells.

Figure 6

HCT116 cells (non-silenced (−) and p38α knock-down (shp38α); with (shC3G) or without C3G knock-down; with (shRap1(1) and shRap1(2)) or without Rap1 knock-down) were used. The effect of p38α/β inhibition by SB203580 (10μM) was also assessed. Anchorage dependent growth assays. Histograms show the mean ± S.E.M. of foci number A. and D. or the number of cells per focus (n = 4) B.. A. and B. *p < 0.05,**p < 0.01,***p < 0.001, compared as indicated. C. Representative images of individual foci. D. Effect of C3G, Rap1 and C3G-Rap1 double knock-down on foci formation. **p < 0.01, ***p < 0.001, versus non-silenced cells; ++p < 0.01 and +++p < 0.001, compared as indicated (n = 3).