Advances in Helicobacter pylori infection involved in gastric cancer metastasis

Gastric cancer is a common cancer of the gastrointestinal tract, highly occurring in East and Southeast Asian. Roughly more than 50% of the population is exposed to Helicobacter pylori (H. pylori) infection worldwide. H. pylori infection is one of the risk factors for gastric cancer and is strongly associated with the development of gastric cancer. The association between H. pylori infection and metastasis of gastric cancer is still inconclusive but has made some progress. For one thing, H. pylori is colonized in the gastric mucosa. The effect of its key virulence factors, VacA and CagA proteins, keeps H. pylori alive in the stomach for a long time and makes it possible for H. pylori to promote the proliferation, epithelial-mesenchymal transition and metastasis of gastric cancer cells. For another, the tumor microenvironment is the site of interaction between host immune system and tumor. By interfering with the effect of tumor cells and immune cells, enhancing the formation of an acidic and hypoxic environment and altering the differentiation of cells in the tumor microenvironment, H. pylori infection can strengthen immune escape and then facilitate the metastasis of gastric cancer. H. pylori infection has become a global public health problem, and its influence on the evolution of gastric cancer cannot be disregarded. The review addresses the correlation between H. pylori infection and gastric cancer metastasis through both key virulence factors and tumor microenvironment. It will provide reference for clinical and basic research in gastric cancer.