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. 2023 Aug 31;24:199. doi: 10.1186/s13059-023-03031-7

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© The Author(s) 2023

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/. 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. 8 — Working model. In AML, HSPC-like leukemic cell populations exhibited one of two known chemoresistance-related expression signatures (LSC and OXPHOS) derived from mouse models (left panel). Among them, HSC-like leukemic cells characterized by the surface marker CD69 possessed chemoresistant capacity possibly via the CD69-mTOR axis. Suppression of the mTOR signaling pathway, in the CD69⁺ HSC-like cell subpopulation and CD69-overexpressing cell lines, might lead to cell quiescence via suppression of cell cycle regulators CCND1 and CDK6 (as shown in Figs. 5a and 6b, and Fig. S5a) and cell adhesion to stromal cells such as MSCs through the CXCR4-CXCL12 interaction (as shown in Fig. 6d, f). Patients with the CD69⁺ HSC-like subpopulation were associated with M0/M1 subtypes and specific genomic alterations and had worse clinical outcomes (right panel)