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Fig. 2 | BMC Cancer

Fig. 2

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. 2

Role of PI3K in melanoma cell growth. Melanoma cells were seeded in 96-well plates (5000 cells/well) and treated 24 h later with inhibitors of (a) ZSTK-474), (b) A66, for 3 days. Cell viability was determined using the sulforhodamine B (SRB) assay. c Response to A66 in NZM lines with PIK3CA variants. d Response to A66 in NZM lines with PIK3R1 variants. BRAF: BRAF-mutant cell lines; RAS: RAS-mutant cell lines; other: cell lines wild-type for both BRAF and RAS. Data were from 2 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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