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. 2022 May 3;11(1):22. doi: 10.1038/s41389-022-00398-3

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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. 4 — PMN-MDSC fuel the proliferation and survival of CTC by providing them with energy-rich lipid vesicles. The proximity of PMN-MDSC to CTC promotes the plasticity of CTC and increases their metastatic potential. In the TME, PMN-MDSCs accelerate their own lipid transfer, uptake, and storage of lipids through increased expression of FATP2, HILDPA, and LOX1 proteins. CTC circulating tumor cell, FATP2 fatty acid transporter protein 2, FFA free fatty acids, HILDPA hypoxia-inducible lipid droplet-associated protein, LOX1 lectin-like oxidized low-density lipoprotein receptor.