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Fig. 1 | Molecular Cancer

Fig. 1

From: PLX8394, a new generation BRAF inhibitor, selectively inhibits BRAF in colonic adenocarcinoma cells and prevents paradoxical MAPK pathway activation

Fig. 1

Effect of the BRAF inhibitors vemurafenib and PLX8394 on the MAPK pathway in colorectal cancer cell lines. Cells were treated with DMSO, vemurafenib at 1 μM, or PLX8394 at 1 μM for 6 h. a, b Representative Western blot of a panel of BRAF wt /KRAS G12D (LM-COL-1, ALA, and LS513) and BRAF V600E /KRAS wt (LIM2405 and COLO 201) colorectal cancer cell lines after treatment with DMSO control or BRAF inhibitors. Western blots were probed for total and phosphorylated MEK1/2 and ERK1/2. The blots are representative of three independent experiments. Total ERK served as a loading control. Western blot signal intensity was quantified and used to measure protein level relative to control. c, d Densitometry of MEK1/2 phosphorylation demonstrating paradoxical activation by vemurafenib in KRAS-mutated cell lines and BRAFi sensitivity in BRAF V600E mutated cell lines LIM2405 and COLO 201. e, f Densitometry of ERK1/2 phosphorylation in the same cell lines as shown in c and d. In panels c–f the total protein:phosphorylated ratio is expressed as the mean ± SD of three independent replicates relative to DMSO-treated control

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Molecular Cancer

ISSN: 1476-4598