Abstract
The aim of this study was to investigate the effect and mechanism of Helicobacter pylori infection in the invasion and metastasis of gastric cancer. Specimens from 80 patients with gastric cancer (of which 20 patients had metastatic gastric cancer) and 40 patients with chronic gastritis were included in this study. H. pylori infection was determined by ELISA and the expression of matrix metalloproteinase-1 (MMP-1) and MMP-10 was observed using immunohistochemistry. The correlation between H. pylori infection and the clinical pathological features of gastric cancer was analyzed by SPSS 13.0 software. The protein expression levels of MMP-1 and MMP-10 in MGC-803 cells infected with H. pylori were analyzed using western blotting. H. pylori infection was found in 62 of the 80 patients with gastric cancer and in 13 of the 40 patients with chronic gastritis. In addition, H. pylori infection was correlated with the staging and lymph node metastasis, but not with the gender, age and histological types of patients. H. pylori infection was also significantly correlated with the expression of MMP-1 and MMP-10 (r=0.8718, P<0.05 and r=0.5477, P<0.05, respectively). The expression of MMP-1 and MMP-10 was significantly upregulated following induction by H. pylori infection (P<0.05), with significant effects occurring following infection for 12 and 6 h, respectively. H. pylori infection may promote the invasion and metastasis of gastric cancer by increasing the expression of MMP-1 and MMP-10.
Highlights
The development of gastric cancer involves several factors, among which Helicobacter pylori infection is the most important [1]
The expression levels of matrix metalloproteinase‐1 (MMP‐1) and Matrix metalloproteinases (MMPs)‐10 were significantly higher in the gastric cancer specimens than those in the chronic gastritis specimens (P
This study has shown that MMP‐1 and MMP‐10 expression was higher in patients with gastric cancer with metastasis than in those with gastric cancer without metastasis
Summary
The development of gastric cancer involves several factors, among which Helicobacter pylori infection is the most important [1]. H. pylori secretes urease, which damages the gastric mucosal barrier. The H. pylori lipopolysaccharide inhibits the binding of laminin to its receptor, resulting in gastric mucosal injury [2]. The vacuolating toxin gene of H. pylori can change ion permeability, leading to cell degeneration [3], and damage the gastric mucosa, causing erosion or ulceration. H. pylori expresses cytotoxin‐associated gene (Cag) A, which generates a cytotoxic effect and induces inflammatory and immune responses. The deformation and necrosis of mucosal cells and inflammatory infiltration can be observed in H. pylori‐infected lesions, and specific antibodies can be detected in serum [4,5]
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