Document Type : Original Research


1 Dept. pathology, Medical Faculty of Shahed University, Tehran, Iran

2 Dept. Immunology, Medical Faculty of Shahed University, Tehran, Iran

3 Dept. Social Medicine, Medical Faculty of Shahed University, Tehran, Iran


Objective: Helicobacter pylori has a well-established role in the development of gastric cancer. In vitro studies reveal increased proliferation of the gastric mucosa in the presence of H. pylori infection. It has been also shown that production of some cytokines, such as interleukin-1 beta (IL-1b) is increased in H. pylori infection. In addition, IL-1b increases proliferation of gastric epithelial cell in culture study. In this study, The effect of transforming growth factor beta (TGF-b) on gastric epithelial cell proliferation has been examined. Materials and methods: AGS cells were cultured with TGF-b. DNA synthesis was evaluated by bromo-deoxyuridine (BrdU) test and total viable cell numbers by MTT assay. Results: TGF-b decreased DNA synthesis and cell numbers. This effect was both timeand dose-dependent (p<0.05). Both tests, BrdU test & MTT assay revealed this suppressive effect, but it was more evident in BrdU test. Conclusion: TGF-b suppresses proliferation of malignant gastric epithelial cells. It appears that modulatin of tyrosine kinase activity is essential to anti-proliferative effect of TGF-b. Decreased gastric epithelial proliferation due to TGF-β may contribute to the decreased risk of gastric cancer and precancerous lesions in H. pylori-infected individuals or slowing the progression of disease in gastric cancer patients.