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2000
Volume 19, Issue 5
  • ISSN: 1389-2029
  • E-ISSN: 1875-5488

Abstract

Background: is a characteristic stem cell marker that regulates the balance between cell self-renewal and differentiation. Evidence has identified as a pivotal oncogenic regulator in diverse malignancies. However, little evidence uncovers the role of genetic variations of gene in cancer etiology. Objective: The aim of this study was to investigate the association between genetic variants in the gene and lung cancer risk. Methods: Based on a two-stage retrospective study with a total of 1559 patients with lung cancer and 1667 healthy controls, we evaluated the relevance between three putative functional SNPs in the promoter (, -2696T>C[rs7959801], -2297T>C[rs3742038] and -1081C>T[rs34570155]) and lung cancer risk. Results: We found that the SNP rs7959801T>C was significantly associated with lung cancer susceptibility. Compared to those with rs7959801TT wild-genotype, individuals with CT/CC variant genotypes exerted consistently beneficial roles in lung cancer risk in the discovery set (adjusted odd ratios [OR] = 0.67; 95% confidence interval [CI] = 0.57-0.80), and in the validation set (OR=0.69; 95%CI=0.54-0.88). Functional assays indicated that the allele transformation from T to C in rs7959801 of gene arrestingly decreased its transcription activity in vitro. Furthermore, the expression levels of were significantly lower in the patients with CT/CC variants than in those who were with TT genotype. Conclusion: Our findings suggested that the rs7959801T>C polymorphism in the promoter conferred a decreased risk to lung cancer by reducing the expression of and it may be a promising indicator for lung cancer predisposition.

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/content/journals/cg/10.2174/1389202919666171128151544
2018-08-01
2024-12-23
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  • Article Type:
    Research Article
Keyword(s): Case-control study; Genetic variant; Lung cancer; Musashi1;; Promoter; Susceptibility
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