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. 2021 Oct 4;11:19667. doi: 10.1038/s41598-021-99267-z

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© The Author(s) 2021

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 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/.

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The effects of p53 on sensitivity to EGFR-TKIs in H1975 cells. Endogenous p53 was silenced using a Crisper/Cas9 knockout system in H1975 cells. (a) The indicated protein levels were analyzed by immunoblotting. (b) Cells were evaluated for morphologic changes that were consistent with MET using a light microscope. (c,d) Cells were treated with the indicated doses of osimertinib for 72 h, and cell viability was determined using MTT assays and cell counting. (e) Cells were treated with the indicated doses of osimetinib for 6 h, and EGFR-related signaling proteins were analyzed by immunoblotting. (f) Two gefitinib-resistant cells (H1975/OR and H1975/p53^KO/OR) were established as described in the Materials and Methods section. At 3 months after drug exposure, cells were treated with the indicated doses of osimertinib for 72 h, and cell viability was determined using MTT assays. ***p < 0.0005 compared with control.