Abstract: Objective: To study the killing effects of genetically engineered adenovirus (H101) in conjunction withCEA genespecific silencing on EC9706 esophageal carcinoma cells and to explore the internal factors influencing H101sensitivity. Methods: We constructed siRNA expression vectors with multiple sequences targeting CEA and transfectedthem into EC9706 cells. Clones with stable CEA gene silencing were selected (interference group 1 and interference group2). Cells with empty vector and untransfected cells served as the controls for cytotoxicity experiments that were then per-formed with H101. Results: There was an evident decrease in survival rate in interference group 2 compared with thecontrol at any given virus density(P<0.05). Compared with the control group, interference group 1 exhibited decreased sur-vival when the virus density was equal to or less than 1 vp/cell (P<0.05); when the virus density exceeded 1 vp/cell, nosignificant difference was found in cell survival between the two groups (P>0.05). Conclusion: Cell survival was signifi-cantly different between the interference groups and the control group. CEA gene silencing in EC9706 cells can decreaseCEA expression and increase the death rate of cancer cells.