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

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 modula- tion of this condition. This study was to...

Full description

Saved in:
Bibliographic Details
Published inChinese science bulletin Vol. 58; no. 16; pp. 1912 - 1918
Main Authors Zhao, YanHua, Zhang, Min, Yan, Fei, Casto, Bruce C., Tang, XiaoFei
Format Journal Article
LanguageEnglish
Published Berlin/Heidelberg Springer-Verlag 01.06.2013
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary: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 modula- tion of this condition. This study was to investigate the association between Prx 1 and tobacco-induced oxidative stress. The ex- pression of Prx 1 and GST n 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 I and GST ~r in nicotine-treated Tca8113 cells. Nuclear factor kappa B (NF-nB) 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 pmol/L, but the proliferation of the cells decreased at 100 pmol/L. ROS levels increased in all groups treated with nicotine at concentrations of 0.1, 1, 10, or 100 pmol/L for 24 h. Prx 1 and GST n 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-rB was translocated from cytoplasm to nucleus, the expression of NF-KB was increased in nucleus. These results suggest that up-regulation of Prxl expression appears to be associated with tobacco-induced oxidative stress, which may play an important role in the pathogenesis of OSCC.
Bibliography: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 modula- tion of this condition. This study was to investigate the association between Prx 1 and tobacco-induced oxidative stress. The ex- pression of Prx 1 and GST n 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 I and GST ~r in nicotine-treated Tca8113 cells. Nuclear factor kappa B (NF-nB) 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 pmol/L, but the proliferation of the cells decreased at 100 pmol/L. ROS levels increased in all groups treated with nicotine at concentrations of 0.1, 1, 10, or 100 pmol/L for 24 h. Prx 1 and GST n 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-rB was translocated from cytoplasm to nucleus, the expression of NF-KB was increased in nucleus. These results suggest that up-regulation of Prxl expression appears to be associated with tobacco-induced oxidative stress, which may play an important role in the pathogenesis of OSCC.
Prxl, nicotine, oxidative stress, oral squamous cell carcinoma
11-1785/N
ISSN:1001-6538
1861-9541
DOI:10.1007/s11434-013-5779-1