摘要
AIM:To investigate the role of the-347G→GA polymorphism in the progression of colorectal cancer(CRC) .METHODS:We designed a case-control study based on a population of CRC patients in China and normal healthy controls with no history of tumors or inherited diseases.Polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP) analyses were used to genotype the variants,and immunohistochemical staining was performed to measure the expression of E-cadherin in different allele cases among the CRC patients and normal controls.RESULTS:The GA-allele(G/GA heterozygous and GA/GA homozygous) did not increase the risk of CRC compared with the G-allele(OR = 1.232,95% CI = 0.898-1.691) .However,the frequencies of the GAallele were higher in poorly differentiated(P = 0.002) and proximal(P = 0.019) CRC patients than in normal controls.We also observed that E-cadherin expression was lower in poorly differentiated CRC patients than in well differentiated CRC patients(P = 0.001) .Furthermore,E-cadherin expression was lower for the GA-allele than for the G-allele(G/G heterozygous) in CRC patients(P = 0.018) .In contrast,there was no significant difference in E-cadherin expression for the G-allele and GA-allele in normal controls(P = 0.292) .CONCLUSION:The-347G→GA promoter polymorphism in E-cadherin gene is associated with specific CRC features,and may be a prognostic factor rather than a susceptibility factor during the progression of CRC.
AIM： To investigate the role of the -347G→GA polymorphism in the progression of colorectal cancer （CRC）.
METHODS： We designed a case-control study based on a population of CRC patients in China and normal healthy controls with no history of tumors or inherited diseases. Polymerase chain reaction-restriction fragment length polymorphism （PCR-RFLP） analyses were used to genotype the variants, and immunohistochemical staining was performed to measure the expression of E-cadherin in different allele cases among the CRC patients and normal controls.
RESULTS： The GA-allele （G/GA heterozygous and GA/GA homozygous） did not increase the risk of CRC compared with the G-allele （OR = 1.232, 95% CI = 0.898-1.691）. However, the frequencies of the GA- allele were higher in poorly differentiated （P = 0.002） and proximal （P = 0.019） CRC patients than in normal controls. We also observed that E-cadherin expression was lower in poorly differentiated CRC patients than in well differentiated CRC patients （P = 0.001）. Furthermore, E-cadherin expression was lower for the GA-allele than for the G-allele （G/G heterozygous） in CRC patients （P = 0.018）. In contrast, there was no significant difference in E-cadherin expression for the G-allele and GA-allele in normal controls （P = 0.292）.
CONCLUSION： The -347G→GA promoter polymorphism in E-cadherin gene is associated with specific CRC features, and may be a prognostic factor rather than a susceptibility factor during the progression of CRC.
