CXCR4 Mediated Antiapoptotic Mechanisms Of Gastric Cancer Cells

Objectives:In one of the most common malignant tumor in the global scope, a drop in the incidence of gastric cancer earlier, currently ranked fourth, but in our country is still in gastric cancer cases worldwide in the number(42%), in east Asia(including China/Mongolian/Russia/north/South Korea/Japan and other countries) the top of their common cancer. At present, the stomach cancer patients can choose chemical treatment and surgical treatment, but the 5-year survival rate in 50%, lead to the death is one of the main causes of cancer invasion and metastasis of the organization.Visible, understand the related regulation in the process of occurrence, invasion and metastasis of gastric cancer and early intervention and early prediction, to formulate relevant treatment, improving the prognosis of patients have positive significance.The study found that high mature gastric cancer cells can express CXCR4. CXCR4 chemotactic factor CXCL12 and its ligand CXCL12- composed of CXCR4 biological axis, and the value-added, spread of tumor cells, immune rejection and tumor is related to the formation of new blood vessels. But its antiapoptotic mechanisms of gastric cancer cells is unclear, as a result, we use stable expression of CXCR4 gastric cancer SGC- 7901 cells, research CXCL12- CXCR4 biological axis of antiapoptotic mechanisms of gastric cancer cells.The expression of CXCR4 SGC7901 gastric cancer cells under the action of CXCL12 activated PI3K/Akt signal pathway, increase antiapoptotic effect of gastric cancer cells.Methods:1. The first part: The stability of CXCR4 expression of human gastric cancer cells SGC7901 mature, wedding after 48 h, the logarithmic phase cells, change in 0.1%fetal bovine serum nutrient solution culture, divided into control group and experimental group and control group to join the buffer, the experimental group tojoin CXCL12(100 ng/m L) continue to develop, 24 h after using flow cytometry respectively to detect the apoptosis rate, detection of repeated three times.2. The second part: The first part will join training by CXCL12 reagent of gastric cancer cells continue to develop, is divided into the experimental group and control group, control group to join the buffer, the experimental group to join LY294002PI3 K inhibitors(100 nmol/ml) for 1 h, using flow cytometry to detect the apoptosis rate, detection of repeated three times.Results:1. The flow cytometry instrument detection of gastric cancer SGC-7901 cells join CXCL12 reagent and not join CXCL12 reagent rate of gastric cancer SGC-7901 cells apoptosis, were 11.40±2.25、2.53±1.18, difference between statistically significant(t= 6.034, P = 6.034).2. Flow cytometry instrument detection not to join the first part of the PI3 K inhibitors LY294002 cultured SGC-7901 gastric cancer cell and join PI3 K inhibitors LY294002 gastric cancer cell apoptosis rate, 2.47±1.15、6.61±1.37, respectively, the difference between the statistically significant(t = 3.999, P=0.016).Conclusion:The experiment proved that CXCL12-CXCR4 biological axis mediated by the activation of PI3K/Akt signal pathway of antiapoptotic effect of gastric cancer cells,promote cancer cells spread, the effect of specific transfer, CXCL12-CXCR4 biological axis to promote cancer cells spread, the mechanism of the effect of specific transfer provide theoretical research.