Mechanisms of arsenic induced gastric cancer

Abstract

Arsenic is a heavy metal element and has been classified as group 1 carcinogens. Humans are mainly exposed to arsenic through drinking water. Long-term exposure to arsenic causes carcinomatous and non-carcinomatous lesions, including gastric carcinoma. At present, the known mechanisms of inorganic arsenic exposure leading to the occurrence and development of gastric cancer mainly include oxidative stress, epigenetic changes and immune regulation. Oxidative stress may change the structure and function of the intestinal epithelium, leading to damage to the intestinal mucosal barrier and then carcinoma. Epigenetic changes are mainly manifested in DNA methylation, histone post-translational modification and miRNA expression, which lead to the occurrence and development of gastric carcinoma. Impairment of the normal function of immune cells such as lymphocytes, dendritic cells, and macrophages may lead to dysbiosis of the gastrointestinal microbiota and development of gastric carcinoma.

Keywords

• arsenic|gastric cancer|oxidative stress|epigenetics|immunoregulation