The Investigatation Of The Expressions Of E-cadherin And β-catenin In HCT116-derived Tumors In Nude Mice After The Intervention Of 5-Aza-2'-deoxycytidine

Objective:To observe 5-Aza-2'-deoxycytidine (5-Aza-CdR) induced E-cadherin andβ-catenin gene expressions in HCT116 cells,and search for new treatment target of colon cancerMaterials and methods:The HCT116-derived tumor model in nude mice was established by subcutaneous inoculation. Fifteen nude mice were randomly divided into two groups:the experiment group(n=8)and control group(n=7). Experiment group nude mice were intraperitoneally injected with 5-Aza-CdR while control group nude mice were only given equivalent volume of PBS.The mice were killed at week 4.The E-cadherin andβ-cat expressions of the tumors were detected using immunohistochemistry.Results:At the end of the fourth week, Immunohistochemistry further showed that the protein expressions of E-cadherin andβ-cat were almost not detected in the HCT116-derived tumor cells of the control group while the E-cadherin andβ-cat expressions were detected on the membranes of the HCT116-derived tumor cells of the experiment group.The differences have statistically significance(p<0.05).Conclusion:E-cad andβ-cat play a great role in the genesis and progress of colon cancer.5-Aza-CdR induces HCT116 cells to re-express E-cadherin andβ-catenin.Its mechanism may be that demethylation of the methylated E-cadherin promoter induced by 5-Aza-CdR restores E-cadherin andβ-catenin reexpression.