Carcinogenesis Advance Access published online on January 16, 2004
Carcinogenesis, doi:10.1093/carcin/bgh073
© 2004 by Oxford University Press
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CANCER BIOLOGY
1 Korean Hereditary Tumor Registry, Cancer Research Center and Cancer Research Institute, Seoul National University, Goyang, Gyeonggi, Korea
* Corresponding author. E-mail: park{at}ncc.re.kr.
Received 20 August 2003
; revised 16 November 2003
; accepted 19 December 2003
E-cadherin plays a critical role in epithelial cell-cell adhesion and maintenance of tissue architecture. Loss of E-cadherin expression in humans has been associated with cancer, and a number of cancer-related mutations have been identified. Here, we sought to investigate whether the -347G
The E-cadherin -347G
GA promoter polymorphism and its effect on transcriptional regulation
2 Research Institute and Hospital, National Cancer Center, Goyang, Gyeonggi, Korea
3 Korean Hereditary Tumor Registry, Cancer Research Center and Cancer Research Institute, Seoul National University, Goyang, Gyeonggi, Korea; Research Institute and Hospital, National Cancer Center, Goyang, Gyeonggi, Korea
GA single nucleotide polymorphism affects the transcriptional activity of the E-cadherin gene. First, we measured the promoter activity of the -347GGA polymorphism using a dual luciferase reporter assay and electrophoretic mobility shift assay (EMSA). The dual luciferase reporter assay showed that the GA allele decreased the transcriptional efficiency by 10-fold (p<0.001) compared to the G allele. Similarly, EMSA revealed that the GA allele had a weak transcription factor binding strength compared to the G allele. We then examined the frequency of this polymorphism in familial gastric cancer (FGC) patients by denaturing high-performance liquid chromatography (DHPLC). We found that the E-cadherin genotype (-347G/GA heterozygous or GA homozygous) was associated with FGC patients (p<0.05) compared with the G homozygous genotype. Taken together, these results suggest that the GA allele may cause weak transcription factor binding affinity and low transcriptional activity in E-cadherin expression.
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