The 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 H۲O۲-induced human esophageal squamous cell carcinoma (ESCC) Eca۱۰۹ cell through mediating the Wnt/β-catenin signaling pathway.Materials and Methods: Eca۱۰۹ cells were classified into ۵ groups: Control group, H۲O۲ group, Propofol + H۲O۲ group, Dkk۱ (Dickkopf-۱, Wnt/β-catenin pathway antagonist) + H۲O۲ group, and Propofol + LiCl (Lithium chloride, Wnt/β-catenin pathway agonist) + H۲O۲ 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 Eca۱۰۹ cells.Results: H۲O۲ resulted in the increased nuclear and cytoplasmatic expression of β-catenin, reduced p-GSK۳β expression, up-regulated ROS content, and induced oxidative DNA damage in Eca۱۰۹ cells. Moreover, Eca۱۰۹ cells treated with H۲O۲ 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-۳, as well as the elevated Bcl-۲ were also observed in Eca۱۰۹ cells in the H۲O۲ group, which were reversed by Propofol or Dkk۱. Moreover, Propofol could inhibit the effect of LiCl on activating the Wnt/β-catenin signaling pathway in H۲O۲-induced Eca۱۰۹ cells.Conclusion: Propofol elicits protective effects to inhibit H۲O۲-induced proliferation and metastasis and promote apoptosis of Eca۱۰۹ cells via blocking the Wnt/β-catenin pathway, offering a possible therapeutic modality for ESCC.

Keywords:

Esophageal neoplasms , Hydrogen peroxide , Propofol , Wnt signaling pathway , β-catenin