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. Author manuscript; available in PMC: 2020 Apr 1.
Published in final edited form as: Cancer Res. 2019 Aug 15;79(19):5074–5087. doi: 10.1158/0008-5472.CAN-19-0244

Figure 2. Validation of candidate drug resistance drivers in a panel of human melanoma cell lines.

Figure 2.

Growth of various engineered cell lines was assessed via CellTiterBlue (Promega). The ability of candidates to increase resistance to vemurafenib and vemurafenib plus cobimetinib varied in (A) A375, (B) 451Lu, (C) A101D, (D) SKMEL28. [*corrected p-value ≤ 0.05, fold-change is relative to vector cells treated with 5 µm vemurafenib ± 5 nM cobimetinib for each independent assay]. (E) A brief 12-hour vemurafenib treatment shows distinct patterns in MEK phosphorylation between the DBL- and RAF-driven mechanisms of resistance. Over-expression of either MCF2∆N or VAV1 increases the level of CDC42-GTP (F) and RAC1-GTP (G).