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. 2019 Sep 25;9:953. doi: 10.3389/fonc.2019.00953

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Copyright © 2019 Yang, Liang, Schmid and Peng.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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MEK mediates the key downstream effect in KRAS-mutant lung cancer cells. (A) Drug information incorporated in the Genomics of Drug Sensitivity in Cancer database. (B) Integrative analysis of drug sensitivity data of KRAS-mutant (n = 20) lung adenocarcinoma cells compared to KRAS-wild-type (WT; n = 40) ones. In the volcano plot, the x-axis indicates the IC50 effect, with effect < 0 representing KRAS-mutation sensitive inhibitors (in blue) compared with KRAS-WT ones. The color intensity and the circle size are proportional to significance value (the y-axis). (C) Sensitivity analysis of KRAS-mutant (in red) and WT (in blue) cells to one of the MEK inhibitors, refametinib.