Abstract

Tissue differentiation-inducing non-protein coding RNA (TINCR) is required for normal epidermal differentiation. TINCR is also strongly overexpressed in human gastric cancer (GC) and contributes to carcinogenesis and tumor progression. However, the association between TINCR polymorphisms and the risk of any diseases, such as GC, remains unknown. In the present study, the tag single nucleotide polymorphisms rs8113645, rs2288947, rs8105637, and rs12610531 were analyzed in 602 patients with GC and 602 age- and sex-matched controls. Polymorphisms were genotyped using TaqMan technology. Carriers of variant rs8113645 and rs2288947 alleles indicated reduced risks of GC (p = 0.003 and 0.037, respectively). A allele genotypes of rs8113645 and G allele genotypes of rs2288947 (rs8113645 GA and AA; rs2288947 AG and GG) were also significantly associated with decreased GC risk (p < 0.05). Stratification analysis displayed that the correlations between GC risk and variant genotypes of both rs8113645 and rs2288947were more evident in younger individuals, men, nonsmokers, and individuals from rural areas. We also demonstrated that rs8113645 GA+AA genotype carriers had lower TINCR mRNA expression levels compared with common genotype in both normal and GC tissues (p < 0.05). These results suggest that long non-coding RNA TINCR polymorphisms may be implicated in GC development.

Highlights

  • Gastric cancer (GC) is one of the most familiar cancers globally and leading to the second cause of cancer-associated mortality [1]

  • We demonstrated that rs8113645 GA+AA genotype carriers had lower Tissue differentiation-inducing non-protein coding RNA (TINCR) mRNA expression levels compared with common genotype in both normal and gastric cancer (GC) tissues (p < 0.05)

  • These results suggest that long non-coding RNA TINCR polymorphisms may be implicated in GC development

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Summary

Introduction

Gastric cancer (GC) is one of the most familiar cancers globally and leading to the second cause of cancer-associated mortality [1]. Our previous epidemiological studies of genetic variation had recognized genetic polymorphism as a crucial factor in the development of GC [3,4,5,6]. LncRNAs have received much attention in relation to their diverse biological functions [7]. Many biological processes, such as genomic imprinting, regulation of gene expression, dosage compensation, compartmentalization and nuclear organization, and nuclear–cytoplasmic trafficking are regulated by lncRNAs [8,9,10]. Several studies have demonstrated dysregulation of many lncRNAs in various human diseases and disorders, including GC [11,12,13,14]

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