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. 2020 Mar 16;10:41. doi: 10.1186/s13578-020-00407-1

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© The Author(s) 2020

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. 7 — Erlotinib induces differential degree of induction apoptosis and autophagy among cells harboring different EGFRs. NIH-3T3 cells harboring EGFR WT and mutants were cultured in DMEM containing 4% FBS with different concentrations of erlotinib (0, 0.3, and 5 µM). Immunoblotting shows the effect of erlotinib on molecular markers of apoptosis and autophagy (caspase-3, PARP, LC3-I/II) after 24 h treatment (a) and 48 h treatment (b). Graphic presentations of the fold change of relative LC3-II/LC3-I in cells treated with erlotinib, presented as mean ± SEM (c)