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. 2022 Jul 6;20:300. doi: 10.1186/s12967-022-03498-1

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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 — Sorafenib-resistant primary AML cells showed high expression of autophagy. A, C Primary AML cells with FLT3-ITD mutation from the patients (case #3 and #5) who relapsed on the maintenance sorafenib therapy were resistant to sorafenib. B Primary AML cells with FLT3-ITD + D835Y mutation from the patient (case #4) who relapsed on the maintenance sorafenib therapy were resistant to sorafenib. D Primary AML cells with FLT3-WT from the patient (case #6) who relapsed on the maintenance sorafenib therapy were resistant to sorafenib. E Sorafenib-sensitive primary AML cells from the patients with FLT3-ITD mutation who were continued complete response (CCR) during sorafenib therapy showed decreasing expression of LC3B-II after vs. before the treatment of sorafenib, showing as LC3B-II/I ratio lower than 1 (0.3 in case #1 and 0.2 in case #2). In contrast to the sorafenib-sensitive cells, sorafenib-resistant AML cells from the patients with FLT3-ITD mutation who relapsed on maintenance sorafenib therapy showed increasing expression of LC3B-II after relapse as compared with before the treatment, presenting as LC3B-II/I ratio higher than 1 (2.5 in case #3, 1.5 in case #4, 5.3 in case #5 and 1.3 in case #6). In accordance with the change of LC3B-II/I ratio, the expression of ATG5 decreased, and p62 accumulated in sorafenib-sensitive cells; while just being opposite, ATG5 increased, and p62 degraded in sorafenib-resistant cells after vs. before the treatment of sorafenib