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. 2022 May 28;12:8983. doi: 10.1038/s41598-022-12995-8

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© The Author(s) 2022

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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Expression of AXL and CDCP1 in lung tumors of patients. (a) IHC analysis of AXL or CDCP1 expression in surgically resected tumors of 6 patients (cases #1–6) before chemotherapy. (b) IHC analysis of AXL and CDCP1 in tumors before EGFR TKI treatment and after recurrence (cases #7). (c) Hypothetical model of how osimertinib resistance is acquired. In osimertinib-sensitive cells, the PI3K/AKT pathway driven by EGFR harboring mutEGFR and T790M is highly susceptible to osimertinib. By contrast, in osimertinib resistant cells, expression of the driver EGFR is reduced, accompanied by SRC activation together with enhanced expression of AXL and CDCP1. Enhanced expression of AXL and CDCP1 activates SFK and AKT signaling pathway, resulting in promotion of cell growth and survival.