Abstract

Expression of matrix metalloproteinase-1 (MMP1), an interstitial collagenase regulating the extracellular matrix, plays a major role in carcinogenesis of gastric cancer, a leading cause of death worldwide. In literature, the single-nucleotide polymorphism (SNP) promoter -1607 1G/2G (rs1799750) at the MMP1 gene promoter has been reported to alter its own transcription level. While the importance’s of the genotype of MMP1 promoter -1607 has not yet been studied in gastric cancer in Taiwan, our aim was to investigate MMP1 promoter -1607 genotypes and gastric cancer (GC) susceptibility in central Taiwan population. In the current hospital-based case-control study, the contribution of MMP1 promoter -1607 genotypes to GC risk was investigated among 121 GC patients and 363 gender- and age-matched healthy controls recruited and genotyped by the polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP) methodology. We found that the genotypic and allelic frequencies were not differentially distributed between GC patient and control groups. The variant 1G containing genotypes have interactions with cigarrete smoking behaviors and Helicobacter pylori infection status, but not alcoholism on GC susceptibility determination. Our findings suggest that the variant 1G allele on MMP1 promoter -1607 may contribute to GC carcinogenesis and may be useful for GC early detection and prevention when combined with cigarrete smoking behaviors and Helicobacter pylori infection status.

Highlights

  • Gastric cancer (GC) is the fourth most common cancer and the second most frequent cause of death from cancer worldwide [1, 2]

  • We have investigated the association of matrix metalloproteinase-1 (MMP1) promoter -1607 genotypes, with gastric cancer susceptibility in Taiwan

  • The results demonstrated that the MMP1 promoter -1607 genotypes were not significantly associated with risk of developing gastric cancer in Taiwan (Tables 2, 3)

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Summary

Introduction

Gastric cancer (GC) is the fourth most common cancer and the second most frequent cause of death from cancer worldwide [1, 2]. The incidence of GC varies among different countries as a result of genetic, epigenetic and environmental factors, which the accurate mechanisms for gastric carcinogenesis remained unknown. In addition to those known environmental factors such as unhealthy diets, infectious agents (e.g., Helicobacter pylori) and pre-existing conditions (e.g., pernicious anemia, atrophic gastritis, and intestinal polyps) [3, 4], the inherited genetic variations may play an important role in determining individual susceptibility to GC but are largely unrevealed, especially for the etiology of GC in Taiwan [5,6,7,8,9,10,11,12].

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