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Figure 6 | Molecular Cancer

Figure 6

From: Effects of AKT inhibitor therapy in response and resistance to BRAF inhibition in melanoma

Figure 6

Addition of AKTi upon development of resistance to MAPK inhibitors can provide further growth inhibition in long term culture, while triple treatment from the beginning delays the emergence of resistance. The PTEN -/- cell line M397 (A) and M299 (B) were cultured in 96-well plates in the presence of 200 nM dabrafenib in combination with 2 nM trametinib. On day 41 or day 5 trametinib was replaced with AKTi (indicated by the arrow in the two cell lines respectively). (C) From day 0, M397 was cultured in the presence of 200 nM dabrafenib alone or in combination with 2 nM trametinib or in the presence of triple drugs; 200 nM dabrafenib, 2 nM trametinib and 2.5 uM AKTi. Cell numbers were determined by a MTS-based assay and use of a gradient with known number of cells which allowed the readout of each well to be calculated into a quantitative cell count (Additional file 5: Figure S5). The cell number for each time point represents the average cell number in 60 well replicates for the plates treated with dabrafenib and trametinib, and 120 replicate wells for the AKTi switch plates.

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