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. 2016 Dec 6;7:13701. doi: 10.1038/ncomms13701

Figure 2. ATM loss-of-function in lung cancer cell lines triggers MEK inhibitor sensitivity.

Figure 2

(a) Chemical structures of MEK inhibitors used in this study. (b) Dose–response experiment of ATM knockdown (shRNA1) AALE cells infected with the indicated MEK1 expression vectors and treated with trametinib for 3 days. Data are normalized to vehicle-treated cells. Error bars indicate s.d.'s (n=3). (c) Dose–response experiment of ATM knockdown NCI-H322 cells treated with trametinib for 5 days. Data are normalized to vehicle-treated cells. Error bars indicate s.d.'s (n=3). (d) Effective concentration resulting in 50% growth inhibitory effect (EC50) is depicted for indicated cell line and compound combinations. The EC50 for the unresponsive control NCI-H460 cells was set to 20 μM. (e) Western blot analysis of CRISPR/Cas9 edited NCI-H322 clones. (f) Dose–response experiment of NCI-H322 cells in which both ATM alleles have been inactivated (four KO clones) or unedited control (four WT clones) treated with PD0325901, TAK-733, trametinib or pimasertib for 5 days. Data are normalized to vehicle-treated cells. Error bars indicate s.d.'s (n=3).