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. Author manuscript; available in PMC: 2019 Apr 9.
Published in final edited form as: Cancer Discov. 2017 Sep 18;8(1):74–93. doi: 10.1158/2159-8290.CD-17-0682

Figure 4.

Figure 4

Paradoxical ERK activation by BRAFi potentiates drug addiction in MEKi-resistant MUTNRAS melanoma. (A–B) Western blot levels of p-ERK, ERK, and loading control TUBULIN in MUTNRAS parental and isogenic MEKi-resistant SDR-lines with indicated hrs on MEKi/trametinib (0.1 µM) treatment (A) or in SDR-lines with indicated hrs off MEKi/trametinib (0.1 µM) treatment, with or without BRAFi/vemurafenib (5 µM) treatment (B). (C–D) Clonogenic growth (C) and percentages of annexin V/PI-positive dead cells (D) in MUTNRAS SDR-lines on or off MEKi/trametinib (0.1 µM) for 6 d, with or without BRAFi/vemurafenib (5 µM) Inset for M207 SDR1 off MEKi for 16 d. (E) Levels and/or sub-cellular localization of p-H2AX, PAR, and AIF in cell-death predominant MEKi-addicted R-lines on or off MEKi for 3 d, with or without BRAFi (5 µM) treatment.