Published online Nov 15, 2015. doi: 10.4251/wjgo.v7.i11.328
Peer-review started: April 26, 2015
First decision: June 2, 2015
Revised: July 1, 2015
Accepted: August 30, 2015
Article in press: September 7, 2015
Published online: November 15, 2015
Gastric cancer (GC) is the third leading cause of cancer-related death worldwide. In areas of high prevalence, such as Japan, South Korea and China, most cases of GC are related to Helicobacter pylori (H. pylori), which involves well-characterized sequential stages, including infection, atrophic gastritis, intestinal metaplasia, dysplasia, and GC. Mucins are the most abundant high-molecular-weight glycoproteins in mucus, which is the first line of defense and plays a major role in blocking pathogenic factors. Normal gastric mucosa shows expression of MUC1, MUC5AC and MUC6 that is specific to cell type. However, the specific pattern of MUC1, MUC5AC and MUC6 expression is changed in gastric carcinogenesis, accompanied by de novo expression of secreted MUC2. Recent studies have provided evidence that variations in these mucin genes affect many steps of GC development, such as H. pylori infection, and gastric precancerous lesions. In this review, we focus on studies of the association between polymorphisms in mucin genes and development of GC. This information should be helpful for the early detection, surveillance, and treatment of GC.
Core tip:Helicobacter pylori (H. pylori) infection is the single most important risk factor in the development of gastric cancer (GC), however the etiology of GC involves host and other environmental factors. Genetic and biological evidence highlights the important roles of variations in mucin genes in the development and progression of GC. In this review, we summarize studies of the association between polymorphisms in MUC1, MUC5AC, MUC6 and MUC2 and development of GC, which should be helpful for the early detection, surveillance, and treatment of GC.