The Emerging Role of GC-MSCs in the Gastric Cancer Microenvironment: From Tumor to Tumor Immunity

Table 1

The emerging role of GC-MSCs in the gastric cancer microenvironment.

Critical molecules/cells	Effect	Reference
PDGF-DD	GC-MSC-derived PDGF-DD promoted GC cell proliferation and migration by PDGF-DD/PDGFR-β signaling pathway.	[53]
IL-8	GC-MSC-derived IL-8 enhanced the proliferation, migration, and proangiogenesis ability of GC cells partly by regulating the activation of Akt or Erk1/2 pathway.	[54]
IL-15	GC-MSC-derived IL-15 could promote GC cell migration and epithelial-mesenchymal transition (EMT) by regulating STAT3 in GC cells.	[55]
miR-221	GC-MSC-CM-derived exosome carrying miR-221 regulated the proliferative and migratory ability of GC cells.	[62]
miR-374	miR-374 participated in regulating gastric carcinogenesis.	[63]
miR-155-5p	miR-155-5p inhibition could regulate the transition of BM-MSC into GC-MSC-like cells.	[49]
YAP	YAP expression in GC-MSCs can affect GC growth and progression in vitro and in vivo.	[64]
Neutrophils	GC-MSC-CM remarkably prompted the chemotaxis of neutrophils and skewed them towards the activated state through GC-MSC-CM-derived IL-6 that mediated the activation of STAT3-ERK1/2 signaling in neutrophils, which could promote migration and angiogenesis of GC.	[71]
PBMCs	GC-MSC-CM could obviously reverse the inhibitory effects of peripheral blood mononuclear cells (PBMCs) on the GC growth. And GC-MSC-CM dampened Treg/Th17 balance in PBMCs.	[77]