Distinct Redox Profiles of Selected Human Prostate Carcinoma Cell Lines: Implications for Rational Design of Redox Therapy

Cancers

Luksana Chaiswing¹  Weixiong Zhong¹ 

[1] Department of Pathology and Laboratory Medicine, School of Medicine and Public Health, University of Wisconsin, 1111 Highland Ave., WIMR 7168, Madison, WI 53705, USA; E-Mails:

关键词: ROS/RNS;    redox state;    cell growth;    cell viability;    cell invasion;    PrEC;    PC3;    RWPE1;    WPE1-NA22;    WPE1-NB26;    LNCaP;    LNCaP-C4-2 cell lines;   

DOI  :  10.3390/cancers3033557

来源: mdpi

【 摘 要 】

The effects of several cancer chemotherapeutic drugs and radiation are mediated, at least in part, by oxidative stress. To better understand this process, we analyzed certain biochemical properties affecting reduction-oxidation (redox) balance in normal prostate epithelial cells and several prostate cancer cell lines. Highly aggressive androgen-independent prostate cancer PC3 cells demonstrated significantly higher levels of total antioxidant capacity (AC) and intra- and extracellular glutathione (GSH)/glutathione disulfide (GSSG) ratios when compared with normal prostate epithelial PrEC cells. WPE1-NB26 cells, a prostate cancer cell line derived from immortalized RWPE1 human prostate epithelial cells, demonstrated significantly higher levels of total AC and intra- and extracellular GSH/GSSG ratios, but lower levels of intracellular reactive oxygen/nitrogen species and lipid peroxidation compared with RWPE1 cells. LNCaP-C4-2 cells, a more aggressive prostate cancer derived from less aggressive androgen-responsive LNCaP cells, exhibited higher levels of AC and extracellular GSH/GSSG ratio when compared to LNCaP cells. Specific cell types showed distinct cytotoxic responses to redox-modulating compounds. WPE1-NB26 cells were more sensitive to phenethyl isothiocyanate and tumor necrosis factor (TNF) than RWPE1 cells, while PC3 cells were more sensitive to TNF than PrEC cells. These results are consistent with the hypothesis that cancer cell redox state may modulate responses to redox-modulating therapeutic regimens.

【 授权许可】

CC BY   
© 2011 by the authors; licensee MDPI, Basel, Switzerland.