Effect of Helicobacter pylori eradication on oncogenes and cell proliferation

Helicobacter pylori , the main cause of chronic gastritis, is a class 1 gastric carcinogen. However, it remains unclear whether H. pylori affects molecular alterations in chronic gastritis. Thus, this study was designed to investigate the effect of H. pylori eradication on the expression of human telomerase RNA (hTR), human telomerase reverse transcriptase (hTERT), c-myc and proliferation nuclear cell antigen (PCNA) in H. pylori associated chronic gastritis.

hTR was determined by in situ hybridization, hTERT, c-myc and PCNA were detected by immunohistochemistry using stomach tissues obtained from 39 H. pylori-infected and 21 H. pylori-negative patients with chronic gastritis before and after H. pylori eradication therapy or treatment for symptom relief only.

Levels of hTR, hTERT, c-myc and PCNA were significantly higher in H. pylori-infected mucosa (51.3%, 53.8%, 53.8% and 16.8 +/- 5.8, respectively) when compared to H. pylori-negative mucosa before therapy (19.0%, 23.8%, 28.6%, 8.8 +/- 3.4, respectively; P < 0.05 in all cases). In patients with successful eradication of H. pylori the levels of hTR, hTERT, c-myc and PCNA (55.5%, 59.3%, 59.3%, 16.8 +/- 5.8, respectively) were significantly reduced after the therapy (22.2%, 22.2%, 14.8%, 7.0 +/- 5.0, respectively; P < 0.05 in all cases). In the H. pylori failed eradication and H. pylori-negative groups, there was no statistical difference in all four measurements.

H. pylori infection may induce the overexpression of hTR, hTERT, c-myc and stimulate cell proliferation. Eradication of H. pylori may reverse the aberrant expression of these oncoproteins and thus correct the abnormal cell proliferation.