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. 2022 Jan 15;20:9. doi: 10.1186/s12964-021-00808-w

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© The Author(s) 2022

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. 3 — Pex direct organ-specific metastasis via integrins. Pex can display different integrin proteins on their surface; ITGα₆β₄- and ITGα₆β₁-expressing exosomes preferentially interact with fibroblasts and epithelial cells in lung, and ITGα_vβ₅-expressing exosomes preferentially fuse with kupffer cells in liver. Once uptaken, Pex induce cellular changes in the target organ, thus promoting cancer cell colonization and organ-specific metastasis