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. 2010 Jun 8;102(12):1724–1730. doi: 10.1038/sj.bjc.6605714

Figure 1.

Figure 1

PLX4720 inhibits the growth of melanoma cells harbouring the BRAF-V600E mutation. (A). Increasing concentrations of PLX4720 reduced the growth of melanoma cell lines harbouring the BRAF-V600E mutation (WM35, 1205Lu and WM164), whereas melanoma cell lines that were BRAF wild type were relatively resistant (WM1346, WM1361A and WM1366). Cells were treated with drug (3 nM–30 μM) for 72 h, and cell numbers were quantified using the MTT assay. Bars show s.e. mean. (B) Low doses of PLX4720 are cytostatic in melanoma cells harbouring the BRAF-V600E mutation. 1205Lu cells were treated were either 0.3 or 3 μM PLX4720 for 24 h before being fixed, stained with propidium iodide and analysed by flow cytometry. (C) PLX4720 inhibits MAPK signalling in BRAF-V600E-mutated melanoma cells. Cells were treated with increasing concentrations of PLX4720 (0.03–30 μM, 1 h); proteins were extracted and probed for expression of phospho-ERK (pERK). Blots were stripped once and reprobed for total-ERK to show even protein loading. (D) PLX4720 induces a concentration-dependent reduction in the phosphorylation of the retinoblastoma protein (phospho-RB), induces the cleavage of PARP, stabilises p27 and suppresses the expression of cyclin D1 in WM164 BRAF-V600E-mutated melanoma cells. Cells were treated with increasing concentrations of PLX4720 (3 nM–30 μM) for 24 h, after which time, protein was extracted and resolved by western blotting (C=vehicle control). Blots were stripped once and probed for actin to show equal protein loading.