| Objective: E-cadherin(CDH1), as one of the cadherin members, relates with development,invasion and metastasis of various cancers.Polymorphisms in the promoter and untranslated region of E-cadherin gene have been associated with tumor development and progression,via modifying its transcriptional activity and protein expression level.This study was designed to investigate the association of single nucleotide polymorphisms on the CDH1 gene with the risk of Colorectal carcinoma.Methods: This hospital-based case-control study included 155 cancer patients and 215 healthy controls, recording their case history, personal history and family medical history. Genomic DNA was extracted by using proteinase K digestion followed by a salting out procedure. CDH1 polymorphisms were analyzed by PCR-restriction fragment length polymorphism analysis (RFLP).Statistical analysis was performed using SPSS11.5 software package SPSS Company,Chicago,Illinois,USA).P<0.05 was considered significant for all statistical analyses.Hardy-Weinberg analysis was performed by comparing the observed and expected genotype frequencies in study groups using Chi-square test. Comparison of the CDH1 genotype, allelotype and haplotype distribution in cancer patients and healthy controls was performed by means of two-sided contingency tables using Chi-square test.The CDH1 haplotype frequencies and linkage disequilibrium coefficient were estimated by using EH linkage software and 2LD software. The odds ratio (OR) and 95% confidence Interval (CI) were calculated using an unconditional logistic regression model and adjusted by age and sex accordingly. Comparison of E-Cadherin expression of different 3′UTR+54C/T genotype and different pathological category performed by means of rank test as well Comparison of E-Cadherin expression of different 3′UTR+54C/T genotype was performed by means of two-sided contingency tables using Chi-square test.Results:1 The distribution of the CDH-1 -160 C/A, -347 G/GA, 3′-UTR C/T genotypes in the control group did not significantly deviate from that expected for a Hardy-Weinberg equilibrium.2 There were no significant difference between patients and healthy controls in allelotype distribution of the CDH-1 -160 C/A (χ2=0.004, P=0.951). And there were also no significant difference in genotype distribution of the CDH-1 -160 C/A between patients and healthy controls(χ2=0.10, P=0.922). Compared with the C/C genotype, the carriers of'A'allele were not significantly modified the risk of developing Colorectal carcinoma. The odds ratios were 1.013(95%CI=0.658~1.558).3 There were no significant difference between patients and healthy controls in allelotype distribution of the CDH-1 -347 G/GA (χ2=0.263, P=0.608). And there were also no significant difference in genotype distribution of the CDH-1 -347G/GA between patients and healthy controls (χ2=0.734, P=0.392). Compared with the G/G genotype, the carriers of'GA'allele were not significantly modified the risk of developing Colorectal carcinoma. The odds ratios were 1.206(95%CI=0.795~1.829).4 There were no significant difference between patients and healthy controls in allelotype distribution of the CDH-1 3′UTR+54C/T (χ2=0.915, P=0.339). And there were also no significant difference in genotype distribution of the CDH-1 3′UTR+54C/T between patients and healthy controls(χ2=0.219, P=0.640). Compared with the C/C genotype, the carriers of'T'allele were not significantly modified the risk of developing Colorectal carcinoma. The odds ratios were 1.111(95%CI=0.721~1.713).5 When stratified by smoking status, -160C/A,-347G/GA,3′UTR +54C/T SNP had no significant influence on the risk of CRC. When stratified by family history of LGIC, -160C/A,-347G/GA,3′UTR +54C/T SNP had no significant influence on the risk of CRC. 6 The results of the 2LD program analysis showed that CDH-1–160C/A and–347G/GA polymorphism were link disequilibrium (D'=0.999832 ,SD=0.0018). There were no significant difference distribution of the CDH1 haplotype difference between patients and healthy controls(χ2=0.267, P=0.966). Compared with -160C/-347G haplotype, The other haplotypes would not change onset risk of colorectal carcinoma.Conclusions:1 The CDH1 -160C/A and -347G/GA polymorphism may not be associated with Susceptibility to colorectal carcinoma2 The CDH1 3′UTR +54C/T polymorphism may not be associated with Susceptibility to colorectal carcinoma.3 When stratified by smoking status and family history of LGIC, -160C/A,-347G/GA and 3′UTR +54C/T SNP had no significant influence on the risk of CRC .4 The CDH1 -160C/A and -347G/GA SNP was imperfectly in linkage disequilibrium in healthy controls. The -160C allele tends to be linked to the -347G allele. The -160C/-347G haplotype was the most frequent in the population, which was 56.7%. The haplotype distribution had no influence on the risk of CRC.
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