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Fig. 2 | Molecular Cancer

Fig. 2

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

Fig. 2

The effect of vemurafenib and PLX8394 on proliferation and survival of BRAF wt / KRAS G12D and BRAF V600E / KRAS wt colorectal cancer cell lines. Inhibitors were used at 0 (DMSO control), 0.1, 0.5, and 1 μM. Cell proliferation was measured after 72 h of BRAFi treatment. a–c Proliferation of BRAF wt /KRAS G12D colorectal cancer cell lines after treatment with vemurafenib or PLX8394 at the indicated concentrations. Relative cell numbers are normalized to DMSO-treated control and differences shown as %. The tinted area indicates increased proliferation after treatment with vemurafenib. The Western blot inlay demonstrates the amount of ERK1/2 phosphorylation relative to the DMSO control at the concentration of vemurafenib that resulted in the biggest increase in proliferation. Lines between lanes denote non-adjacent lanes from the same membrane. d–e Inhibition of proliferation in BRAF V600E / KRAS wt colorectal cancer cell lines LIM2405 and COLO 201 after treatment with the indicated concentrations of vemurafenib or PLX8394. All data are shown as mean ± SD of independent triplicates relative to DMSO-treated controls

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Molecular Cancer

ISSN: 1476-4598