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. 2022 Jun 11;41:200. doi: 10.1186/s13046-022-02390-6

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — A subset of EGFR-mutated NCLC cells is highly resistant to icotinib. A Growth-inhibitory effects of indicated time and doses of icotinib were determined via CCK-8 assays, IC50s are depicted. B Clonogenic assays detected the response of EGFR-mutated NSCLC cells to icotinib. C Cell apoptosis induced by icotinib was displayed by flow cytometry analysis (Annexin V-7-AAD staining in the x-axis and PI in the y-axis). D Cleaved Caspase-3 and Cleaved PARP known as the markers of apoptosis were measured using immunoblotting assays. [In line charts, **P < 0.01, ***P < 0.001 as compared with the control group. In bar charts, **P < 0.01, ***P < 0.001 as compared with the 24 h group, ##P < 0.01vs. the 48 h group, §§ P < 0.001 as compared with the 72 h group]