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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. 1 — PCCS: Pancreatic cancer cells. PCCs and PSCs are based on the mechanism of interaction between sEVs. Pancreatic cancer-derived sEVs activate the LIN28B /let-7/HMGA2/PDGFB signaling pathway by expressing LIN28B, and recruit PSCs from afar to promote the formation of pre-metastatic niches. Secondly, the expression of miR-1246 and miR-1290 sEVs formed an inflammatory environment of niche by promoting the expression of PSCs fibrosis and other related genes. Conversely, miR-5703 expressed on PSCS-derived sEVs activated the PI3K/Akt pathway, miR-21 enhanced RAS /ERK signaling activity, and in anoxic environment: Both miR-4465 and miR-616-3p ultimately promoted the proliferation and metastasis of pancreatic cancer by inhibiting the PTEN/ Akt pathway