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. 2021 Mar 31;20:59. doi: 10.1186/s12943-021-01347-1

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© The Author(s) 2021

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. 2 — CTCs interactions with constituents of the blood circulation. CTCs are exposed to a number of influencing factors while in circulation including fluid sheer stress (FSS), hypoxia, nutrient starvation/glucose metabolism. Platelets, coagulation proteins and immune cells provide either direct or indirect contacts with CTCs to aid in their survival. Platelets are a rich source of TGF-β which promotes EMT. Platelets and coagulation proteins also protect CTCs from FSS through the creation of a rich microthrombi surrounding CTCs. CTCs evade immune detection through the expression of immune decoy receptors such as CD47 and PD-L1. These cells, proteins and circulating nucleic acids/extracellular vesicles can influence not only the phenotype of the CTC in circulation but also its molecular make up and cellular fate within the peripheral blood circulation