Expression of NFkappaB p65 and its target genes in gastric cancer and precancerous lesions

Objective To study the expression of NFκB p65 and its target genes in intestinal metaplasia (IM), dysplasia (Dys), gastric cancer (GC) infected with Helicobacter pylori (Hp) and explore the mechanism of infection by cytotoxin-associated antigen A expressing Hp (CagA~+Hp) in the development of gastric cancer. Methods CagA antibody in blood sample of 289 patients was determined by ELISA. Hp was detected by rapid urease test and Warthin starry staining. Expression of NFκB p65 and its target genes in IM, Dys and GC was examined by immunohistochemistry. Results In IM Ⅰ～Ⅱ, IMⅢ, DysⅠ, DysⅡ～Ⅲ and GC, the expression of NFκB p65 was significantly higher in patients with CagA~+Hp infection than those without CagA Hp infection. In IMⅢ and DysⅡ～Ⅲ, the expression of NFκB p65, c-myc, CyclinD_1 and bcl-xl was significantly higher in patients with CagA Hp infection than those without CagA Hp infection. In gastric cancer infected with CagA~+Hp, the expression of NFκB p65, c-myc, CyclinD_1 and bcl-xl was significantly higher in intestinal type than in diffuse type. Conclusion There are different mechanisms in intestinal type and diffuse type in the development of gastric cancer. The occurrence of intestinal type gastric cancer is associated with CagA~+Hp infection which by NFκB p65 upregulating the expression of c-myc, CyclinD_1, bcl-xl in patients with IMⅢ, DysⅡ～Ⅲ. It may be an effective method to prevent gastric cancer by inhibiting NFκB p65.