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. 2020 Jan 6;8(1):7. doi: 10.3390/biomedicines8010007

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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The roles of gastric cancer stem cells (GCSCs) in the immune microenvironment. Stromal cells can support GCSC development through various kinds of interactions. Tumor-associated macrophages (TAMs) enhance the induction of VEGF and COX2/PGE2 in GCSCs through monocyte chemoattractant-1 (MCP-1) and milk-fat globule-epidermal growth factor-VIII (MFG-E8). Cancer-associated fibroblasts (CAFs) not only directly enhance the CSC capabilities of GCSCs by activating the Smad2 pathway (TGF-β inhibitors inhibit this process) but also attract macrophages that are converted into TAMs by CXCL12. GCSCs can inhibit T cell activity through the PD-L1/PD-1 interaction. Some theories suggest that GCSCs affect the balance of Treg and Th17 subsets, and GCSCs impair the function of dendritic cells (DCs). The solid line represents strong evidences supporting theory in GCSC; the dashed line represents possible evidences guide theory in GCSC.