| Objective : To Explore the Epstein-Barr virus(EBV), Helicobacter pylori cagA (H. pylori cagA ) and vacA genes (H. pylori vacA )infections in the tumorigenesis of gastric carcinoma,and also to investigate the relationship between EBV infection, H.pylori cagA and vacA infection in the development of gastric carcinoma.To study the effects of Epstein-Barr virus(EBV) on proliferation and apoptosis of gastric epithelia cell cultured in vitro .Methods:①Dividing 46 cases of Gastric cancer patients proven by pathology into experimental group, 43 cases of precancerous lesions (including IM, atrophic gastritis and dysplasia, etc) patients also proven by pathology into the control group, to take gastric tissue by endoscope, using PCR amplification method to detect EBV-DNA which is in gastric cancer and precancerous lesions, using rapid urease test to detect H.pylori, and then do genotyping which were detected as positive patients .②To culture a certain number of the B95-8 cell line in vitro, and extract EBV from the cells, then preserve the EBV in -70℃.③When gastric epithelia cells SGC-7901 cultured in vitro climb on the glass slide, put EBV with the concentrations of 3.5×102/ml,3.5×103/ml,3.5×104/ml respectively, after 48 hours, and then use the SABC method to detect expression change of ki-67 in SGC-7901 cells.④To culture the SGC7901 cell line in vitro and inoculate the cells to six-well plates with the cell density of 3×104/ml, culture after 24h, put into the EBV with the concentrations of 3.5×102/ml,3.5×103/ml,3.5×104/ml, culture after 48 hours, and then, respectively, make the single cell suspension to detect the apoptosis rate with Flow cytometry.Results:①There were 12 samples of EBV infection in 89 samples of specimens.The total positive rate was 13.5% (12/89), and the EBV were not detected in the adjacent tissues.There were significant differences between experimental group(21.7%) and control group(4.7%) (X2= 5.56, P<0.05). Statistical analysis showed that EBvaGC (EBV associated gastric carcinoma, EBVaGC) and EBV-negative gastric cancer (EBV negative gastric careinoma, EBVnGC) were not significantly different in pations age and degree of gastric careinoma differentiation( P>0.05), however, difference was obvious in terms of pations gender,EBV positive rate was higher in male than the female (X2 = 3.93, P<0.05).②EBV infection had positive effect from chronic atrophic gastritis to gastric ulcer to IM to gastric cancer.(r = 0.25465 p = 0.0160).③H.pylori positive rate was 60.9% (28/46) in the experimental group,and 60.9% (28/46) in the control group, there was significant difference between the two groups by X2 test(X2 = 4.98, P <0.05).④Using X2 to test H.pylori cagA and vacA in experimental group and control group (X2 = 5.42, P <0.05; X2 = 3.97, P <0.05), the difference was statistically significant.⑤In terms of patients gender and age, there were no differences in HP, cagA, vacA gene positive and negative rate between experimental group and control group(P> 0.05), and in terms of the degree of tumor differentiation there was significantly different in H. pylori ,cagA,vacA gene positive and negative rate between the to two groups. (P <0.01.).⑥EBV infection was Positively correlated to cagA (P0.0287, r=0.23199),and not correlated to vacA (P=0.8094, r= 0.02595).⑦Obviously, EBV promote the proliferation and expression of ki-67 of the SGC7901 cell line, and inhibit its apoptosis.Conclusion:①EBV infection is related to tumorigenesis of gastric carcinoma and is male Predominant,but not related to patient's age,degree of tumor differentiation.②H.pylori cagA+ and vacA+ infection are related to tumorigenesis of gastric carcinoma ,especially Pathological differentiation,but not related to patient'sgender,age.③EBv infection is Positively correlated to cagA ,but not correlated to vacA .④Obviously, EBV promotes the proliferation and inhibit the apoptosis of the gastric epithelia cell cultured in vitro.
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