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. 2019 Aug 23;9:12329. doi: 10.1038/s41598-019-48243-9

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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AK4 signaling helped the response of EGFR inhibitors. (a) Correlation plot of AK4 expression level and AUC of Erlotinib in COSMIC lung adenocarcinoma cell lines. Specific cell lines were presented in black. (b) Correlation plot of AK4 expression level and AUC of Erlotinib in COSMIC lung adenocarcinoma cell lines. Specific cell lines were presented in black. (c) The expression level of AK1, AK4, pEGFR, and EGFR in H358 and Hcc827 cells after shAK4 treatment. Beta-actin was used as loading control. (d) The cell viability assay of Erlotinib in H358-shLuc, H358-shAK4-1 and H358-shAK4-2 cells. (e) The cell viability assay of Afatinib in H358-shLuc, H358-shAK4-1 and H358-shAK4-2 cells. (f) The cell viability assay of Erlotinib in Hcc827-shLuc, Hcc827-shAK4-1 and Hcc827-shAK4-2 cells. (e) The cell viability assay of Afatinib in Hcc827-shLuc, Hcc827-shAK4-1 and Hcc827-shAK4-2 cells.