Abstract
Mesenchymal stem cells (MSCs) have been considered as one of the key components of tumor microenvironment and are believed to play critical roles in cancer progression. MSCs within tumor microenvironment acquire novel functions that are not observed in normal MSCs. Emerging evidence suggest that tumor-resident MSCs could skew immune cells to a tumor-promoting phenotype, leading to the escape from immune surveillance. As neutrophils are predominant innate immune cells, we recently explored the interaction between tumor-resident MSCs and neutrophils. Our results revealed that tumor-resident MSCs regulate the chemotaxis, survival, activation, and function of neutrophils in gastric cancer through the IL-6–STAT3 signaling pathway. Intriguingly, neutrophils activated by tumor-resident MSCs could strongly induce the differentiation of normal MSCs into CAFs, forming a feedback loop to synergistically prompt cancer progression. Our findings indicate that the regulation of neutrophil biology and function by tumor-resident MSCs may present a novel mechanism for the role of MSCs in remodeling cancer microenvironment and provide a potential target for the treatment of gastric cancer.
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