Nicotine-induced upregulation of antioxidant protein Prx 1 in oral squamous cell carcinoma

Abstract

Nicotine is a source of exogenous oxidative stress, which is associated with the pathogenesis of numerous diseases including oral squamous cell carcinoma (OSCC), whereas an antioxidant protein, peroxiredoxin 1 (Prx 1), plays an important role in the modulation of this condition. This study was to investigate the association between Prx 1 and tobacco-induced oxidative stress. The expression of Prx 1 and GST π in OSCC Tca8113 cells, which were pre-treated with nicotine, was determined. In the present study, MTT assay, reactive oxygen species (ROS) assay, RT-PCR and Western blot analyses, respectively, were conducted to assess cell viability, ROS level, and expression level of Prx 1 and GST π in nicotine-treated Tca8113 cells. Nuclear factor kappa B (NF-κB) expression was detected by immuno-fluorescence. Our results showed the growth of Tca8113 cells was increased in a dose-dependent manner when cells were treated with nicotine at concentrations from 0.1 to 10 μmol/L, but the proliferation of the cells decreased at 100 μmol/L. ROS levels increased in all groups treated with nicotine at concentrations of 0.1, 1, 10, or 100 μmol/L for 24 h. Prx 1 and GST π mRNA and protein expression were up-regulated in cells treated with nicotine for the same time at different concentrations or at the same concentration for different times (P<0.05). NF-κB was translocated from cytoplasm to nucleus, the expression of NF-κB was increased in nucleus. These results suggest that up-regulation of Prx1 expression appears to be associated with tobacco-induced oxidative stress, which may play an important role in the pathogenesis of OSCC.