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. 2021 May 24;11:652378. doi: 10.3389/fonc.2021.652378

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Copyright © 2021 Gao, Li, Xu, Zhang, Huang, Dai and Liu

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Roles of exosomes in gastric cancer pre-metastatic niches. Exosomes contribute to pre-metastatic niche formation through multiple mechanisms, including (A) immunosuppression by facilitating TAM and TAN polarization, inhibiting dendritic cell maturation and T cell activation, and inducing MDSCs, (B) stroma remodeling by acting on stromal cells such as CAF and MSCs and ECM balance, (C) angiogenesis, (D) MMT and apoptosis of tissue-specific cells, such as PMCs, and (E) organotropisms. The liver is drawn to represent a metastatic target. CAF, cancer-associated fibroblast; DC, dendritic cell; ECM, extracellular matrix; EMT, epithelial-mesenchymal transition; GC, gastric cancer; MDSCs, myeloid-derived suppressor cells; MMT, mesothelial-mesenchymal transition; MSC, mesenchymal stem cell; PMC, peritoneal mesothelial cell; TAM, tumor-associated macrophage; TAN, tumor-associated neutrophil; Th17, T-helper 17 cell; Treg, regulatory T cell.