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Regulation of CagA-Helicobacter on Gastric PIM2 Expression in Gastric Cancer
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AbstractInfection with cagA-positiveH. pylori has been linked to an increased risk of gastric cancer. However, the precise mechanism by whichcagAregulates PIM2 expression in gastric cancer is currently unknown. To address this issue, a mutant NCTC11637ΔcagA strain ofH. pyloriwas 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 ofH. pyloriinfection.
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Title: Regulation of CagA-Helicobacter on Gastric PIM2 Expression in Gastric Cancer
Description:
AbstractInfection with cagA-positiveH.
pylori has been linked to an increased risk of gastric cancer.
However, the precise mechanism by whichcagAregulates PIM2 expression in gastric cancer is currently unknown.
To address this issue, a mutant NCTC11637ΔcagA strain ofH.
pyloriwas 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 ofH.
pyloriinfection.
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