The Study Of The Relation Between Expression Of RUNX3 Protein And Helicobacter Pylori Infection In Gastric Carcinoma

RUNX3 was found in 1995 by a Japanese scientist ,as a gene that can promote digestive enzyme secretion. Recent years RUNX3 has been described at home and abroad as a tumor suppressor that frequently shows loss of expression due to hemizygous deletion and hypermethylation in gastric cancer.Meanwhile Helicobacter pylori infection is also a significant contributory factor during gastric carcinogenesis , however, the working group of International Agency for Research on Cancer (1ARC) classified it as a class I carcinogen. But How chronic Helicobacter infection leads to malignancy has emerged as a major global research interest,the exact molecular biological mechanism is to be investigated ,and what is the relationship of Runx 3 to the major environmental gastric carcinogen Helicobacter pylori? These questions attract many scientists.The present study is to discuss if Hp infection is related with RUNX3 expression during the development and progression of gastric cancer.Methods: We would deploy Rabbit Anti-RUNX3--a rabbit polyclonal antibody and Streptavidin-Peroxidase (SP) immunohistochemistry to detect RUNX3 expression in Hp(-) and Hp(+)gastric mucosal specimens obtained from patients with chronic superficial gastritis ,chronic atrophic gastritis and gastic carcinoma. Results:RUNX3 expression in various human gastric mucosa tissue was analyzed. It demonstrates that RUNX3 expression rate in chronic superficial gastritis mucosa is 74.19%, and 64.29%, 27.59% in chronic atrophic gastritis mucosa and gastric carcinoma tissue respectively. Compared with that in the chronic superficial gastritis mucosa, the overall expression level of RUNX3 in the gastric cancer tissues was significantly lower (P<0.1); In the group of chronic superficial gastritis, the difference in RUNX3 expression between the Hp (-) gastric mucosa and Hp (+) gastric mucosa isn't statistical significant (P>0.1), nor is it in the group of chronic atrophic gastritis, but the difference is constantly changing, and in the group of gastric carcinoma, it was clear that the Hp (+) gastric tissue specimens had a loss or drastic decrease of RUNX3 expression as compared with Hp (+) gastric tissue specimens. Concolusion: inactivation of RUNX3 plays a vital role in the genisis and progression during the process of chronic superficial gastritis→chronic atrophic gastritis→gastic carcinoma, and maybe during the development RUNX3 inactivation is due to Helicobacter pylori infection .