The Investigation Of The Expressions Of Cx32 And Cx43 In HCT116-derived Tumors In Nude Mice After The Intervention Of 5-Aza-2′-deoxycytidine

Objective:5-Aza-2'-deoxycytidine(5-Aza-CdR) is an inhibitor of DNA methyltrans ferase;it may reactivate methylated antioncogene, therefore, inhibit the growth of cancer cells.This tudy was to observe the inhibitory effect of 5-Aza-CdR on the expressions of Cx32and Cx43 of the colon cancer xenografts in nude mice, explore the possible mechanisms, and search for new treatment target of colon cancer.Materials and methods:The model of human HCT116-derived tumor in nude mice was constructed.Fifteen nude mice were randomly divided into two groups:the experiment group(n=10)and control group(n=10).Experiment group nude mice were treated with 5-Aza-CdR.The mice were killed at week 4 and the protein expression of Cx32 and Cx43 was detected by immunohis tochemistry.Results:Low expression of Cx32 and Cx43 protein were found in HCTl 16 cells xenografts in nude mice without treatment of 5-Aza-CdR. After treatment, the expression of Cx32 and Cx43 proteins in xenografts HCT116 cells were increased.The Differences have statistically significance (p<0.05).Conclusion:Cx32 and Cx43 played an important role in the genesis and progressof colon cancer.5-Aza-CdR may reactivate antioncogene Cx32 and Cx43 silenced by denovo-Methylation.This result was consistent with Our previous study found that the deletion of the Cx32 gene in colon cancer cell line HT-29 was related with its methylation status of promoter region.5-Aza-CdR may provide a new way to the treatment of the colon cancer.