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. 2022 Jan 28;13(1):92. doi: 10.1038/s41419-022-04531-3

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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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — A PKH26-labeled hucMSC-exo was uptaken by K562-R cells. Scale bar: 50 μm. B–E The expression of USP6 and miR-146a-5p in K562-R cells treated by different hucMSC-exo concentrations (0, 50, 100, and 200 μg/mL) for 24 h. F Flow cytometry analysis of apoptosis of K562-R cells treated by hucMSC-exo (100 μg/mL) alone or in combination with 1 μM IM for 48 h. G Flow cytometry analysis of apoptosis of USP6-overexpressing K562-R cells treated by hucMSC-exo (100 μg/mL) alone or in combination with 1 μM IM for 48 h. In vivo tumor formation assays. K562-R was administered to each mouse. On day 90, mice were sacrificed and (H) spleen weight, (I) white-blood cell count, and (J) survival curve were analyzed. *P < 0.05, **P < 0.01, ***P < 0.001.