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Fig. 6 | BMC Cancer

Fig. 6

From: Diverse mechanisms activate the PI 3-kinase/mTOR pathway in melanomas: implications for the use of PI 3-kinase inhibitors to overcome resistance to inhibitors of BRAF and MEK

Fig. 6

Role of mTOR in melanoma cell proliferation. Melanoma cells were seeded in 96-well plates (5000 cells/well) and treated 24 h later with inhibitors of (a) KU-0063794 and (b) NVP-BEZ235. Cell viability was determined using the sulforhodamine B (SRB) assay. c, d Five parental melanoma lines, their vemurafenib resistant (PR for NZM7, 12, 20, 22 and 49) and the respective drug withdrawn cells were tested for their sensitivity to mTOR inhibitor (c) KU0063794 and (d) mTOR plus PI3K dual inhibitor NVP-BEZ235. BRAF: BRAF-mutant cell lines; RAS: RAS-mutant cell lines; other: cell lines wild-type for both BRAF and RAS. Data were from 3 to 4 independent experiments performed in duplicates. Yellow areas represent the concentration ranges between the biochemical IC50 and 100 x IC50 values of inhibitors for their specific targets; x-axis represents cell-based EC50 values; y-axis represents inhibition % at 100 μM of the corresponding inhibitors where 100% inhibition indicates complete stop of cell growth

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BMC Cancer

ISSN: 1471-2407

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