Protective effect of propofol on hydrogen peroxide-induced human esophageal carcinoma via blocking the Wnt/β-catenin signaling pathway

OBJECTIVE(S): To analyze the potential influences of propofol on the oxidative stress of H(2)O(2)-induced human esophageal squamous cell carcinoma (ESCC) Eca109 cell through mediating the Wnt/β-catenin signaling pathway. MATERIALS AND METHODS: Eca109 cells were classified into 5 groups: Control group, H(2)O(2) group, Propofol + H(2)O(2) group, Dkk1 (Dickkopf-1, Wnt/β-catenin pathway antagonist) + H(2)O(2) group, and Propofol + LiCl (Lithium chloride, Wnt/β-catenin pathway agonist) + H(2)O(2) group. Western blotting was performed to determine the protein expressions, flow cytometry to measure the content of ROS, immunofluorescence staining to detect the oxidative DNA damage, as well as MTT, AnnexinV-FITC/PI, Wound-healing, and Transwell assays to test the biological characteristics of Eca109 cells. RESULTS: H(2)O(2) resulted in the increased nuclear and cytoplasmatic expression of β-catenin, reduced p-GSK3β expression, up-regulated ROS content, and induced oxidative DNA damage in Eca109 cells. Moreover, Eca109 cells treated with H(2)O(2) alone had enhanced cell proliferation and metastasis but decreased cell apoptosis, as compared with those without any treatment; meanwhile, the declined Cyt C, Bax, and cleaved caspase-3, as well as the elevated Bcl-2 were also observed in Eca109 cells in the H(2)O(2) group, which were reversed by Propofol or Dkk1. Moreover, Propofol could inhibit the effect of LiCl on activating the Wnt/β-catenin signaling pathway in H(2)O(2)-induced Eca109 cells. CONCLUSION: Propofol elicits protective effects to inhibit H(2)O(2)-induced proliferation and metastasis and promote apoptosis of Eca109 cells via blocking the Wnt/β-catenin pathway, offering a possible therapeutic modality for ESCC.