| Background:Gastric cancer is one of the most malignant tumors that threaten people's health. Along with the improvement of socio-economic situation, the downdraft of high incidence and mortality has been observed. However, gastric cancer is still the most common tumor. Therefore, to clarify the molecular mechanism of gastric cancer is of great importance for the prevention of the disease.In spite of the pathogen and pathogenesis of gastric cancer is not clear, numerous studies have showed that the disease is mediated by many cytokines. On the other hand, the formation of tumor is based on the immunity environment and the increase of immune escape ability. For this reason, researchers throw their eyes to the auto-immune mechanism of the body, they try to use the endogenous immuno-competence to eliminate tumor, which could be a supplement of the treatment of tumor. Lymphocytes play an important role in the anti-tumor immunological effect, and helper T cell is essential to the Immune Response, immunological memory and killing tumor cell.IL-2 is expressed by T lymphocyte (Th1 type), the biologic activity is very important. It is the essential cytokine that ensure the normal immunologic function. IL-2R is the receptor of IL-2; it functions after combines with IL-2. So far, many researches have revealed that IL-2 and IL-2R show antitumor effect. JAK/STAT is the most important signal transduction pathway of IL-2. JAK is a protein phosphatase, the substrate is STAT protein. More and more studies showed that STAT3 was in tyrosine phosphorylation persistent state in patients with tumor. The excessive activation of STAT3 could lead to target gene expression imbalance, which then lead to the out control of cell growth. Therefore, to study the state of activation of JAK-STAT is important to elucidate the pathogenesis of gastric cancer. In this study, the blood level of IL-2,IL-2R in healthy people and patients with gastric cancer was observed and compared. Besides, in cellular level, rhIL-2 and AG490, the specific inhibitor of JAK was added to the cell culture medium, in order to study the role of JAK-STAT3 signal transduction pathway in the development of gastric cancer.Objective:To study the blood level of IL-2,IL-2R in healthy people and patients with gastric cancer. RhIL-2 was added in the culture system of gastric carcinoma cell line AGS, and observe the effect on the cell growth. AG490, the specific inhibitor of JAK was added to the cell culture medium, in order to study the role of JAK-STAT3 signal transduction pathway in the development of gastric cancer.Methods:To analyze the clinical data of the patients of early stage of gastric cancer during October 2008 to May 2009, blood serum was collected and separated, the level of IL-2 and IL-2R was determined by ELISA. Gastric carcinoma cell line AGS were cultured, rhIL-2 was added to the culture system, the proliferation activity was analyzed by XTT method. AG490, the specific inhibitor of JAK was added to the cell culture medium, the proliferation activity was also analyzed by XTT method, and western blotting was used to determine the expression level of JAK protein, STAT3 protein and p-STAT3.Results:1. The blood level of IL-2 and IL-2R in patients with early stage of gastric cancer was significantly decreased than normal healthy people.2. RhIL-2 could inhibit the AGS cell proliferation in a concentration depended manner.3. The specific inhibitor of JAK as AG490 could inhibit the AGS cell proliferation in a concentration depended manner.4. AG490 could inhibit the expression of JAK protein, STAT3 protein and p-STAT3.Conclusion:The level of IL-2 and IL-2Rin blood could reflect the immunologic function of patients with early stage of gastric cancer, which may be the cause of immunologic escape, and that lead to the cause of tumor or transfusion of tumor. Besides, JAK-STAT3 signal transduction pathway participates in the biological behaviour. |
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