rs187960998 polymorphism in miR-211 prevents development of human colon cancer by deregulation of 3'UTR in CHD5.

Background: Previous research indicated that overexpression of miRNA-211 could promote colorectal cancer cell growth by targeting tumor suppressive gene Chromodomain-helicase-DNA-binding protein 5 (CHD5) in human colon cancer (CC). Moreover, the function of the single-nucleotide polymorphism (SNP) located in the mature region of miR-211 has not been investigated. In this study, we found that SNP of rs187960998 in miR-211 was involved in the occurrence of CC by acting as a tumor suppressor by mal-regulation of its target gene CHD5. Materials and methods: The genotype of total 685 CC patients was detected by real-time PC R, the proliferation of CC cell lines with different genotypes of miR-211 was determined by Cell Counting Kit-8, cell invasion evaluated by transwell and the activity of the CHD5 promoter in CC cell lines transfected with different miR-211 was determined by luciferase assay. The expression of CHD5 in CC patients was determined by the immunohistochemistry, and the relapse-free survival rate was analyzed by Kaplan-Meier analysis. Results: C/T SNP of miR-211 could inhibit CC cell proliferation and invasion by upregulation of C HD5. And SNP in rs187960998 of mi R-211 was associated with tumor size, metastasis and tumor differentiation in CC patients. Patients with CC genotype have significantly low CHDS expression than the T-carrier, while no significant expression difference in miR-211 expression among different genotype subsets. Patients with CC genotype have significantly shorter postsurgery survival rate compared to the T-carrier. Conclusion: rs187960998 in miR-211 was highly associated with a decreased risk of CC in the Chinese population by deregulating a tumor suppressive gene CHD5.