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. Author manuscript; available in PMC: 2019 Jan 1.
Published in final edited form as: Mol Cancer Ther. 2017 Nov 13;17(1):73–83. doi: 10.1158/1535-7163.MCT-17-0196

Figure 6. Silencing of IGF1R or ACK1 enhances suppression of pS6 when combined with trametinib.

Figure 6

A: (Upper panel) Expression of ALK in the eight BRAF/NRAS-WT melanoma cell lines. Western Blot shows expression of ALK and GAPDH. (Lower panel) Silencing of ALK in SK-MEL-23 cells does not affect viability +/− trametinib in cell survival assays. Cells were treated with siRNA for 24h and then with ALK siRNA or non-silencing control alone and in the presence of trametinib (10nM) for 72h. Cell numbers were measured by MTT assay. B: Silencing of IGF1R in WM1963 leads to enhanced pS6 suppression when combined with trametinib. Cells were treated with siRNA for 24h and then with vehicle or drug for 24h. Numbers are the densitometry values corresponding to pS6/tS6. C: (Upper) Silencing of ACK1 enhances the suppression of pS6 in WM209 and SK-MEL-23 cells when combined with trametinib. Cells were treated with siRNA for 24h and then with vehicle or drug for 24h before Western blot analysis for pERK and pS6. (Lower) Western Blot shows the expression of ACK1 across the cell line panel. D: Combined silencing of ACK1 and IGF1R suppresses pS6 signaling in combination with trametinib (10nM). WM3681 and M257 Cells were treated with siRNA as above and then with trametinib for 24h before Western blot analysis for pERK and pS6.