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. 2019 Apr 19;11(4):562. doi: 10.3390/cancers11040562

Figure 3.

Figure 3

Targeting p90 ribosomal S6 kinase (RSK) by LJI308 inhibits phosphorylation of YB-1 at S102 in CRC cells. (A) KRAS wild-type SW48 and KRAS(G13D)-mutated HCT116 cells were treated with increasing concentrations of the RSK inhibitor, LJI308, for 20 h. The level of YB-1 phosphorylation was analyzed by Western blotting. (B) The mean ratio of phospho-YB-1 to YB-1 was evaluated by densitometry under unstimulated basal conditions in the indicated number of experiments in KRAS wild-type SW48 and KRAS(G13D)-mutated HCT116 cells (C) as well as in CaCo2 cells with and without conditional expression of the KRAS(G12V) mutation in the indicated number of experiments. (B,C) Representative Western blots are shown. Asterisks indicate a statistically significant difference in the phosphorylation of YB-1 between the indicated cells/conditions (*** p ≤ 0.001 and **** p ≤ 0.0001).