Abstract
Background and aimsMicroRNAs (miRNAs) are known for their function as translational regulators of tumor suppressor or oncogenes. Single nucleotide polymorphisms (SNPs) in miRNAs related genes have been shown to affect the regulatory capacity of miRNAs and were linked with gastric cancer (GC) and premalignant gastric conditions. The purpose of this study was to evaluate potential associations between miRNA-related gene polymorphisms (miR-27a, miR-146a, miR-196a-2, miR-492 and miR-608) and the presence of GC or high risk atrophic gastritis (HRAG) in European population.MethodsGene polymorphisms were analyzed in 995 subjects (controls: n = 351; GC: n = 363; HRAG: n = 281) of European descent. MiR-27a T>C (rs895819), miR-146a G>C (rs2910164), miR-196a-2 C>T (rs11614913), miR-492 G>C (rs2289030) and miR-608 C>G (rs4919510) SNPs were genotyped by RT-PCR.ResultsOverall, SNPs of miRNAs were not associated with the presence of GC or HRAG. We observed a tendency for miR-196a-2 CT genotype to be associated with higher risk of GC when compared to CC genotype, however, the difference did not reach the adjusted P-value (odds ratio (OR) - 1.46, 95% confidence interval (CI) 1.03-2.07, P = 0.032). MiR-608 GG genotype was more frequent in GC when compared to controls (OR −2.34, 95% CI 1.08–5.04), but significance remained marginal (P = 0.029). A similar tendency was observed in a recessive model for miR-608, where CC + CG vs GG genotype comparison showed a tendency for increased risk of GC with OR of 2.44 (95% CI 1.14–5.22, P = 0.021). The genotypes and alleles of miR-27a, miR-146a, miR-196a-2, miR-492 and miR-608 SNPs had similar distribution between histological subtypes of GC and were not linked with the presence of diffuse or intestinal-type GC.ConclusionsGene polymorphisms of miR-27a, miR-146a, miR-196a-2, miR-492, miR-492a and miR-608 were not associated with the presence of HRAG, GC or different histological subtypes of GC in European subjects.
Highlights
Despite decreasing incidence of gastric cancer (GC) in most developed countries, GC accounted for a total of 989,600 new cases and 738,000 deaths in 2008 worldwide [1]
Helicobacter pylori (H. pylori) infection in gastric mucosa may lead to the development of atrophic gastritis (AG) and intestinal metaplasia (IM) and is a cardinal risk factor for development of GC [2]
A number of gene alterations have been implicated in gastric carcinogenesis, but none of them has been yet transferred to daily clinical practice due to the lack of association strength [4]
Summary
Despite decreasing incidence of gastric cancer (GC) in most developed countries, GC accounted for a total of 989,600 new cases and 738,000 deaths in 2008 worldwide [1]. Helicobacter pylori (H. pylori) infection in gastric mucosa may lead to the development of atrophic gastritis (AG) and intestinal metaplasia (IM) and is a cardinal risk factor for development of GC [2]. The development of gastric adenocarcinoma cannot be explained by the presence of H. pylori alone. Recent data suggest a potential influence of single nucleotide polymorphisms (SNPs) of microRNA-related genes (miRNAs) for the risk of cancer development [5]. Single nucleotide polymorphisms (SNPs) in miRNAs related genes have been shown to affect the regulatory capacity of miRNAs and were linked with gastric cancer (GC) and premalignant gastric conditions. The purpose of this study was to evaluate potential associations between miRNA-related gene polymorphisms (miR-27a, miR-146a, miR-196a-2, miR492 and miR-608) and the presence of GC or high risk atrophic gastritis (HRAG) in European population
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