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Polymorphisms in RETN gene and susceptibility to colon cancer in Saudi patients.

ABSTRACT: Resistin is an adipocytokine, which has been studied for its role in insulin resistance and recently in inflammation. Several single-nucleotide polymorphisms (SNPs) have been identified in the human resistin gene (RETN). This study aims to investigate the association of RETN rs1862513 (C-420G) and rs3745367 (G+299A) SNPs with the colon cancer risk in Saudi patients.This is a case-control study conducted among Saudi adult colon cancer patients recruited from King Abdulaziz Hospital and Oncology Center in Jeddah, Saudi Arabia.In this study, 120 Saudi volunteers (60 colon cancer patients and 60 disease-free controls) were studied. The SNPs were determined by polymerase chain reaction (PCR) and genotyping using PCR- restriction fragment length polymorphism analysis.In comparing the result obtained for the patient group with that of the controls, colon cancer group displayed different genotype distribution of the RETN C-420G and G+299A SNPs. The study indicated that the SNP-420 heterozygous (CG) genotype (odds ratio [OR]=2.48, 95% CI 1.07-5.74, P=.03) and the SNP +299 heterozygous (GA) genotype (OR=6.5, 95% CI 1.77-24.18, P=.002) significantly increased the risk of colon cancer. A further analysis of the genotype combination of SNPs RETN C-420G and G+299A showed a larger increase in the colon cancer risk.These preliminary results suggested a potential role for RETN C-420G and G+299A polymorphisms in the genetic predisposition to colon cancer disease.

SUBMITTER: Alharithy RN

PROVIDER: S-EPMC6152568 | biostudies-literature | 2014 Jul-Aug

REPOSITORIES: biostudies-literature

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Polymorphisms in RETN gene and susceptibility to colon cancer in Saudi patients.

Alharithy Rowyda N RN

Annals of Saudi medicine 20140701 4

<h4>Background and objectives</h4>Resistin is an adipocytokine, which has been studied for its role in insulin resistance and recently in inflammation. Several single-nucleotide polymorphisms (SNPs) have been identified in the human resistin gene (RETN). This study aims to investigate the association of RETN rs1862513 (C-420G) and rs3745367 (G+299A) SNPs with the colon cancer risk in Saudi patients.<h4>Design and setting</h4>This is a case-control study conducted among Saudi adult colon cancer p ...[more]

PMID: 25811207

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Project description:Background:Inflammation is a fundamental factor that contributes to the development and progression of several types of cancer including colon cancer. Toll-like receptors (TLRs) and their signaling pathways have been reported to be associated with chronic inflammation and thereby induced cancer. Our aim was to investigate the expression and polymorphisms of TLR2 and their association with colon cancer. Methods:Real-time PCR and immunohistochemistry were used to investigate TLR2 gene expression and to evaluate the potential risk of predisposition to colon cancer caused by three tagging single-nucleotide polymorphisms (SNPs) on TLR2, including rs3804100, rs4696480, and rs3804099. TaqMan assay was conducted on samples from 115 patients with colon cancer and 102 age- and sex-matched normal individuals. Results:We found that, TLR2 was highly expressed in epithelial colon cancer cells and both TLR2 mRNA and protein levels, and significantly decreased in tumor tissues compared to normal tissues. Two of three TLR2 SNPs increased the risk of colon cancer. However, TLR2 rs3804099 increased the risk of colon cancer development by more than 3.8- and 5-fold in female patients and patients aged less than 57 years, respectively. The T allele of TLR2 rs3804100 showed a significant association with patients less than 57 years. In silico analysis of the TLR2 nucleotide substitution in SNP rs3804100 and rs3804099 determined that 67% and 70% probability of these single nucleotide variants alter splicing phenotypes, rs3804100 more specifically result on activating an additional splice site. Genotype and allele frequencies of rs4696480 were similar between the overall study populations. Thus, TLR2 rs4696480 appear to be not involved in colon cancer in our study population. Conclusions:There was a significant link between innate immunity deregulation through disruption of the TLRs and potential development of colon cancer. These SNPs can be used as screening markers for predicting colon cancer risk earlier in life to implement necessary prevention.

Project description:BackgroundN-acetyltransferase 2 (NAT2) metabolizes arylamines and hydrazines moeities found in many therapeutic drugs, chemicals and carcinogens. The gene encoding NAT2 is polymorphic, thus resulting in rapid or slow acetylator phenotypes. The acetylator status may, therefore, predispose drug-induced toxicities and cancer risks, such as bladder, colon and lung cancer. Indeed, some studies demonstrate a positive association between NAT2 rapid acetylator phenotype and colon cancer, but results are inconsistent. The role of NAT2 acetylation status in lung cancer is likewise unclear, in which both the rapid and slow acetylator genotypes have been associated with disease.MethodsWe investigated three genetic variations, c.481C>T, c.590G>A (p.R197Q) and c.857G>A (p.G286E), of the NAT2 gene, which are known to result in a slow acetylator phenotype. Using validated PCR-RFLP assays, we genotyped 243 healthy unrelated Caucasian control subjects, 92 colon and 67 lung cancer patients for these genetic variations. As there is a recent meta-analysis of NAT2 studies on colon cancer (unlike in lung cancer), we have also undertaken a systematic review of NAT2 studies on lung cancer, and we incorporated our results in a meta-analysis consisting of 16 studies, 3,865 lung cancer patients and 6,077 control subjects.ResultsWe did not obtain statistically significant differences in NAT2 allele and genotype frequencies in colon cancer patients and control group. Certain genotypes, however, such as [c.590AA+c.857GA] and [c.590GA+c.857GA] were absent among the colon cancer patients. Similarly, allele frequencies in lung cancer patients and controls did not differ significantly. Nevertheless, there was a significant increase of genotypes [c.590GA] and [c.481CT+c.590GA], but absence of homozygous c.590AA and [c.590AA+c.857GA] in the lung cancer group. Meta-analysis of 16 NAT2 studies on lung cancer did not evidence an overall association of the rapid or slow acetylator status to lung cancer. Similarly, the summary odds ratios obtained with stratified meta-analysis based on ethnicity, and smoking status were not significant.ConclusionOur study failed to show an overall association of NAT2 genotypes to either colon or lung cancer risk.

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Polymorphisms in RETN gene and susceptibility to colon cancer in Saudi patients.

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Polymorphisms in RETN gene and susceptibility to colon cancer in Saudi patients.

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