Objective: This study was to investigate inhibiting effect of structurally unique Second mitochondria-derived activator of caspase (Smac) in combination with cisplatin on esophageal cancer cell line ECA109.
Methods: PcDNA3.1-Smac (ECA109/Smac group), pcDNA3.1 (ECA109/neo group) and PBS (ECA109 or control group) were transfected into ECA109 cells respectively, and transfected cells which expressed Smac stably were got. Smac protein expression was analyzed by Western blot. The invasive ability of cells was examined. Flow cytometry was used to analyze apoptosis induced by cisplatin with Annexin V/PI double staining technique.
Results: Smac gene was successfully transfected into ECA109 cell, over-expression of Smac could decrease cell invasive ability obviously compared to control group (P<0.05). Apoptosis rate of cells induced by cisplatin in ECA109/Smac group was significant higher than that in ECA109/neo and ECA109 group (P<0.05).
Conclusion: It indicated that over-expression of Smac increases the sensitivity of esophageal cancer ECA109 cells to cisplatin treatment, combination of conventional anticancer drug with Smac may be beneficial for the treatment of esophageal cancer.
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