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. 2017 Mar 6;8(15):25395–25417. doi: 10.18632/oncotarget.15915

Figure 1. Mechanisms of acquired resistance displayed by vemurafenib-resistant clones and populations obtained from A375, 501 Mel and SK-Mel-28 cells.

Figure 1

(a) Table that lists vemurafenib-resistant clones (C) and populations (P) and the corresponding resistance mechanism. The full list of known alterations that were searched for is reported in Supplementary Table 2. The resistance mechanism of SK-Mel-28 P1 population remains to be discovered. (b) Western blot for BRAFV600E protein in A375 parental cell line and vemurafenib-resistant clones (C) and populations (P). SK-Mel-197 cells, which are wt for BRAF, are included as a negative control. Immunoblotting for α-TUBULIN (TUB) is used as loading control. (c) Cartoon depicting the BRAFV600E splicing variants identified in A375 vemurafenib-resistant clones and populations. RBD: RAS-binding domain. (d) Electropherograms showing a single-nucleotide mutation (A→C) in the KRAS gene of A375 P2 resistant population (right) compared to A375 parental cell line (left), resulting in the K117N amino acid substitution. (e) Western blot for BRAFV600E protein in 501 Mel parental cell line and vemurafenib-resistant population (P1). SK-Mel-197 cells, which are wt for BRAF, are included as negative control. Immunoblotting for α-TUBULIN (TUB) is used as loading control. (f) Cartoon depicting the BRAFV600E splicing variant identified in 501 Mel P1. (g) In SK-Mel-28 C1 and C2 vemurafenib-resistant clones, EGFR and PDGFRβ are over-expressed, as detected by real-time PCR. The graphs represent the mean±SEM of 3 independent experiments. *p<0.05, **p<0.01.