The Expression And Significance Of MiRNA-100 In H.pylori Infected Gastric Diseases

Objective: Here we detected the expression of mi RNA-100 in gastric cancer tissues of H.pylori infection and non H.pylori infection. Likewise, its differential expression was assayed in precancerous lesions tissues of gastric cancer and chronic gastritis gastric tissues which were infected by H.pylori or not. Compared the difference expression of mi RNA-100 in different groups, and further investigated the relevance between the expression of mi RNA-100 and clinicopathological characteristics. The correlation of expression between mi RNA-100 and H.pylori infection in gastric cancer tissues, precancerous lesions tissues of gastric cancer and chronic gastritis gastric tissues samples was analyzed to research the function of mi RNA-100 and H.pylori in gastric cancer deeply. The potential targets of mi RNA-100 were predicted and identified to explore the molecμ Lar mechanism of the incidence of gastric cancer.Methods: A total of 30 gastric cancer tissues, 10 precancerous lesions tissues of gastric cancer and 30 chronic gastritis gastric tissues samples were examined. Apply rapid urease test and detect HP antibody in serum to determine the infection of H.pylori or not. Stem-loop primer reverse transcription and Taqman real time PCR were used to access the abundance of mi RNA-100 in different gastric tissue samples.The aberrant expression of mi RNA-100 in gastric cancer tissues and precancerous lesions tissues of gastric cancer and chronic gastritis gastric tissues was analyzed. The potential targets of mi RNA-100 were predicted by bioinformatics methods and were identified by reporter vector systems. Adhibit SPS S 20.0 to accomplish the whole statistics, and paired group t test and non-paired group t test was performed to determine if this difference was statistically significance or not. The nμ Ll hypothesis was rejected at the 0.05 level.Results:(1) The relative expression of mi RNA-100 was markedly increased in thegastric cancer tissues than in the precancerous lesions tissues of gastric cancer, and was significantly increased in the gastric cancer tissues than in the chronic gastritis gastric tissues, and was observably increased in the precancerous lesions tissues of gastric cancer than in the chronic gastritis gastric tissues.(2) The level of mi RNA-100 had correlation with the TNM, but no correlation with other clinicopathological characteristics(clinical stages, lymph node metastasisstages and tumor stage, etc).(3) In 30 gastric cancer tissues samples, the relative expression of mi RNA-100 was significantly increased in the H.pylori infected gastric cancer tissues than in the non ones.(4) In 10 precancerous lesions tissues of gastric cancer samples, the relative expression of mi RNA-100 was significantly increased in the H.pylori infected samples than in the non ones.(5) In 30 Chronic superficial gastritis tissues samples, the relative expression of mi RNA-100 between H.pylori infected samples and non. H.pylori infected samples had statistical significance.(6) HS3ST2 may be the target gene of mi RNA-100,dual luciferase assay report suggested that the expression of mi RNA-100 can inhibit HS3ST2 and regulate the expression of HS3ST2 in gastric cancer cell MGC-803.Conclusion:(1) The aberrant expression of mi RNA-100 has a firm relationship with the pathogenesis of gastric cancer, maybe it acts as a tumor promoting gene in gastric cancers.The expression of mi RNA-100 in patients’ gastric cancer tissues has no significant correlation with patients’ TNM stage, lymph node metastasis and other clinical and pathological features.(2) High expression of the mi R-100 in H.pylori infected gastric cancer and precancerous lesions tissues of gastric cancer shows that H.pylori infection might be a trigger factor for an abnormal expression of mi RNA-100 in gastric cancer. This may be one of the molecμ Lar mechanism of H.pylori infection induced gastric cancer.(3) HS3ST2 is the target gene mi RNA-100, and its expression in human gastric cancer MGC-803 cell was regulated by mi RNA-100.