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. 2022 Jan 21;11(1):6. doi: 10.1038/s41389-022-00380-z

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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. 7 — Pro-tumor phenotype of MM-MSCs is associated to a metabolic rewiring and an increased ability to donate mitochondria. Furthermore, myeloma PCs increase the expression of CX43 and CXCL12 proteins in stromal cells with consequent activation of the corresponding receptor CXCR4, which favors mitochondrial uptake from MSCs. The high mitochondrial trafficking in MM microenvironment supports tumor to escape PI-induced intracellular oxidative stress and mitochondrial damage.