Release of pro-inflammatory mediators and increased local levels of oxygen and nitrogen species can contribute to carcinogenesis. The dysregulated production of cytokines in inflammatory MI 192 microenvironment stimulates the expression of genes associated with cancer development and modifies structural features of microenvironment to accelerate cancer initiation and progression. Tumor microenvironment consists of various stromal cells, including infiltrating immune cells, carcinoma-associated fibroblasts, mesenchymal stem cells, and blood and lymphatic vascular networks. These cells interact with each other and constitute inflammatory microenvironment and contribute to tumorigenesis. Among the stromal cells, macrophages, as important immune regulatory cells, play a dominant role in managing inflammation in tumor microenvironment. For example, macrophages isolated from tumor microenvironment of breast cancer patients secret chemotactic cytokines to augment metastasis of carcinoma cells. Macrophages have also been shown to promote inflammatory response and tumorigenesis through impacting on expression of inflammatory cytokines and altering the molecular oncogenic programs within epithelial cells. Mesenchymal stem cells are another major component of the tumor microenvironment and are considered as the precursor cells of cancer associated mesenchymal cells and endothelial cells. The previous studies have indicated that MSCs secret soluble factors to promote cancer cell proliferation and metastasis. In an inflammation-associated gastric cancer model, MSCs could be activated towards CAFs to increase chronic inflammation and cancer progression. Furthermore, MSCs have been reported to recruit monocytes/macrophages to promote tumor ML 141 growth in a CCR2-depedent manner. Interactions between macrophages and MSCs produce an activated, pro-inflammatory phenotype with high CXCL10 and IL-6 secretion, which may influence the inflammatory microenvironment. Gastric cancer is a classic model of chronic inflammation to cancer. However, the role of MSCs activated by macrophage in gastric cancer and the underlying mechanism are still largely unknown. In this study, we found that MSCs were strongly activated by macrophages under inflammatory condition, to produce inflammatory cytokines and tumor-promoting factors, leading to the enhancement of gastric epithelial cell and cancer cell proliferation and migration through the activation of NF-kB pathway.