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. 2022 Jan 3;20:1. doi: 10.1186/s12964-021-00806-y

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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. 3 — Mechanism of targeted metastasis of pancreatic cancer to liver and lung. Upon arrival in the liver, sEVs derived from pancreatic cancer first express the integrin αVβ5 they carry, which promotes the release of pro-inflammatory factor S100A8 by activating Kupffer cells, making the liver an inflammatory environment. The CD44v6/C1QBP complex carried by sEVs also has the same mechanism by phosphorylating insulin-like growth factor 1 signaling molecules, thereby initiating the development of liver fibrosis. Secondly, the sEVs secreted by fibroblasts promote the expression of serum amyloid protein and STAT3 by releasing the pro-inflammatory factor IL-6 and binding to the IL-6 receptor on the liver, and the liver becomes an inflammatory and immunosuppressive environment by recruiting immunosuppressive cells. SEVs ITGα6β4 and ITGα6β1 bind to lung cells and epithelial cells and regulate lung specific metastasis by forming an inflammatory environment in the lung