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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. 4 — Inhibition of autophagy enhanced suppression of sorafenib on FLT3 downstream signaling and pro-apoptotic effect in both Ba/F3-ITD and Ba/F3-ITD + D835 mutated cells. A In Ba/F3-ITD cells, after autophagy was inhibited with CQ, sorafenib more markedly suppressed FLT3 downstream signaling of significantly induced cleaved caspase-3. B In Ba/F3-ITD + D835Y cells, without CQ co-treatment, sorafenib could only down-regulate the expression of p-FLT3, but not FLT3 downstream signaling, and no apparent cleaved caspase-3 was induced. After being dealt with CQ, autophagy was inhibited, sorafenib significantly suppressed the downstream signaling of FLT3 and up-regulated the expression of cleaved caspase-3