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. Author manuscript; available in PMC: 2021 Sep 1.
Published in final edited form as: Clin Cancer Res. 2020 Nov 23;27(5):1476–1490. doi: 10.1158/1078-0432.CCR-20-2860

Figure 5.

Figure 5.

YM-254890 and MEKi lead to sustained MAPK inhibition in UVM cells. (A) Viability curves for four UVM cell lines treated with increasing doses of YM in combination with four doses of trametinib (left) and corresponding HSA synergy diagrams (right). (mean ± SEM, n = 3). (B) Growth assays of Mel202, OMM1.3, MP41, and OMM1 cells treated with vehicle, YM, trametinib, or Combo. (C) Mel202 and OMM1.3 sum Z scores of Pratilas_MAPK are shown (top) with heatmaps (bottom) showing expression of individual signature genes (mean ± SEM, n = 2). (D) Expression counts (log2) of DUSP6, SPRY2, and SPRY4 from RNA-seq data for Mel202 and OMM1.3 cells (mean ± SEM, n = 2). (E) Western blot analysis of indicated proteins in Mel202, (F) OMM1.3, and (G) MP41 cells. Cells were treated with vehicle, YM, trametinib, or Combo for 4, 24, 48, and 72 hours.