Abstract
Recent studies explored the association between insulin receptor substrate-2 (IRS-2) gene rs1805097 polymorphism and colorectal cancer (CRC) with contradictory findings. Therefore, we conducted a comprehensive meta-analysis by searching the databases of PubMed and Embase. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by using fixed-effect or random-effect models. A total of 5 citations containing 6 case-control studies involving 4,333 cases and 5,333 controls were included. Our data indicated that IRS-2 rs1805097 polymorphism was associated with decreased risk of CRC. Stratification analysis of ethnicity found that rs1805097 polymorphism decreased the risk of CRC among Americans. Stratification analysis of cancer type suggested that this polymorphism decreased the risk of colon cancer. In summary, this meta-analysis indicates that IRS-2 gene rs1805097 polymorphism plays an important role in the pathogenesis of CRC.
Highlights
Colorectal cancer (CRC) is the second most commonly diagnosed cancer worldwide [1]
We yielded a total of 51 citations after initial search. 33 citations were removed after removing duplicates and screening the titles and abstracts. 18 citations were selected for further full text review. 13 citations were excluded: 1 investigated other polymorphisms; 5 were about other diseases; 2 were meta-analyses
Our data indicated that the findings of this meta-analysis were stable and trustworthy (AA vs. GG+GA, Figure 5). Both Egger's and Begg's tests (A vs. G, Figure 6) revealed that there was no obvious publication bias for rs1805097 polymorphism. In this current meta-analysis, we found that IRS2 gene rs1805097 polymorphism decreased the risk of colorectal cancer (CRC)
Summary
Colorectal cancer (CRC) is the second most commonly diagnosed cancer worldwide [1]. CRC is one of the primary causes of cancer-related mortality. Some environmental factors including diet, cigarette smoking, physical inactivity, and alcohol consumption, are considered to influence the risk of CRC [2]. Studies demonstrated that those environmental factors through the insulin pathway are significantly associated with the risk of CRC [3, 4]. Several researches provided evidence to support that insulin is associated with the risk of CRC [3, 4]. Animal research found that insulin enhances the growth of aberrant crypt foci, CRC precursor lesions, and increases the number and the size of the tumors [4]
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