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Functional polymorphism at the miR-502-binding site in the 3' untranslated region of the SETD8 gene increased the risk of prostate cancer in a sample of Iranian population. | LitMetric

Functional polymorphism at the miR-502-binding site in the 3' untranslated region of the SETD8 gene increased the risk of prostate cancer in a sample of Iranian population.

Gene

Cellular and Molecular Research Center, Zahedan University of Medical Sciences, Zahedan 98167-43181, Iran; Department of Clinical Biochemistry, School of Medicine, Zahedan University of Medical Sciences, Zahedan 98167-43181, Iran. Electronic address:

Published: August 2017

MicroRNAs (miRNAs), a class of non-coding RNAs, bind to the 3' untranslated regions (3'-UTRs) of target mRNAs and regulate gene expression. Genetic variations in miRNA binding domains influence the susceptibility to several diseases such as cancer. Several studies investigated the impact of single-nucleotide polymorphism (SNP) rs16917496 T>C within the 3'-UTR of SETD8 on cancer susceptibility, but the results were controversial. In addition, no study has been conducted to inspect the impact of this SNP in prostate cancer (PCa). Thus, the present study aimed to find out the possible association between rs16917496 polymorphism at the 3'UTR of SETD8 and PCa risk. This case-control study was done on 169 patients with pathologically confirmed PCa and 182 benign prostatic hyperplasia (BPH). Genotyping was done using PCR-RFLP method. The findings revealed that rs16917496 variant significantly increased the risk of PCa in codominant (OR=2.54, 95%CI=1.50-4.30, p<0.001, TC VS TT and OR=3.03, 95%CI=1.63-5.66, p<0.001, CC vs TT), dominant (OR=2.86, 95%CI=1.62-4.43, p<0.001, p<0.001). The C allele significantly increased the risk of PCa (OR=1.72, 95%CI=1.28-2.33, p<0.001) compared to T allele. In conclusion, the findings indicated that rs16917496 polymorphism may be a risk for predisposition to PCa in an Iranian population. Further studies with larger sample sizes and different ethnicities are required to confirm our findings.

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http://dx.doi.org/10.1016/j.gene.2017.05.060DOI Listing

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