Regulation of CagA-Helicobacter on Gastric PIM2 Expression in Gastric Cancer

Abstract Infection with cagA-positive H. pylor i has been linked to an increased risk of gastric cancer. However, the precise mechanism by which cagA regulates PIM2 expression in gastric cancer is currently unknown. To address this issue, a mutant NCTC11637ΔcagA strain of H. pylori was constructed, and the effects of H. pylori/cagA on PIM2 expression in gastric cancer cells (HGC27, SGC7901, and AG) were examined. The results showed that co-culturing gastric cancer cells with NCTC11637 significantly increased PIM2 expression levels (P < 0.001) compared to the control group. Additionally, the expression of PIM2 in cells co-cultured with NCTC11637 was higher than that co-cultured with NCTC11637ΔcagA (P < 0.001). Furthermore, the eukaryotic expression vector pcDNA-cagA was successfully constructed, and its transfection into gastric cancer cells resulted in a significant increase in PIM2 mRNA expression levels compared to the control group after 48 hours. These findings suggest that H. pylori /CagA may play a crucial role in regulating PIM2 expression and therefore may contribute to the pathogenesis of H. pylori infection.