GPx3 promoter hypermethylation is a frequent event in human cancer and is associated with tumorigenesis and chemotherapy response

被引:91
作者
Chen, Baishen [1 ,3 ]
Rao, Xi [4 ]
House, Michael G. [1 ]
Nephew, Kenneth P. [1 ,5 ]
Cullen, Kevin J. [2 ]
Guo, Zhongmin [1 ,5 ]
机构
[1] Indiana Univ Sch Med, Med Sci Program, Bloomington, IN USA
[2] Univ Maryland, Sch Med, Marlene & Stewart Greenebaum Canc Ctr, Baltimore, MD 21201 USA
[3] Sun Yat Sen Univ, Dept Surg, Mem Hosp, Sch Med, Guangzhou 510275, Guangdong, Peoples R China
[4] Indiana Univ, Interdisciplinary Biochem Grad Program, Dept Mol & Cellular Biochem, Bloomington, IN USA
[5] Indiana Univ, Simon Canc Ctr, Indianapolis, IN 46204 USA
关键词
DNA methylation; Antioxidant enzymes; Head and neck cancer; Chemotherapy response; Prognosis; S-TRANSFERASE-PI; NITRIC-OXIDE SYNTHASE; OXIDATIVE DNA-DAMAGE; NECK-CANCER; PROSTATE-CANCER; BREAST-CANCER; CELL-LINES; GLUTATHIONE; HEAD; EXPRESSION;
D O I
10.1016/j.canlet.2011.05.013
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Glutathione peroxidase 3 (GPx3), a plasma antioxidant enzyme, maintains genomic integrity by inactivating reactive oxygen species (ROS), known DNA-damaging agents and mediators of cancer chemotherapy response. In this study, we demonstrate that loss of GPx3 expression by promoter hypermethylation is frequently observed in a wide spectrum of human malignancies. Furthermore, GPx3 methylation correlates with head and neck cancer (HNC) chemoresistance and may serve as a potential prognostic indicator for HNC patients treated with cisplatin-based chemotherapy. Our findings support the hypothesis that defects in the antioxidant system may contribute to tumorigenesis of a wide spectrum of human malignancies. GPx3 methylation may have implications in chemotherapy response and clinical outcome of HNC patients. Published by Elsevier Ireland Ltd.
引用
收藏
页码:37 / 45
页数:9
相关论文
共 51 条
[1]  
[Anonymous], 2006, J CARCINOG, DOI DOI 10.1186/1477-3163-5-14
[2]   DNA methylation and gene silencing in cancer [J].
Baylin S.B. .
Nature Clinical Practice Oncology, 2005, 2 (Suppl 1) :S4-S11
[3]  
Behrend L, 2003, BIOCHEM SOC T, V31, P1441
[4]   Glutathione peroxidases in different stages of carcinogenesis [J].
Brigelius-Flohe, Regina ;
Kipp, Anna .
BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS, 2009, 1790 (11) :1555-1568
[5]   The relationship between cisplatin-induced reactive oxygen species, glutathione, and BCL-2 and resistance to cisplatin [J].
Brozovic, Anamaria ;
Ambriovic-Ristov, Andreja ;
Osmak, Maja .
CRITICAL REVIEWS IN TOXICOLOGY, 2010, 40 (04) :347-359
[6]   Oxidative damage in an esophageal adenocarcinoma model with rats [J].
Chen, XX ;
Ding, YW ;
Yang, GY ;
Bondoc, F ;
Lee, MJ ;
Yang, CS .
CARCINOGENESIS, 2000, 21 (02) :257-263
[7]   Dietary antioxidants during cancer chemotherapy: Impact on chemotherapeutic effectiveness and development of side effects [J].
Conklin, KA .
NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL, 2000, 37 (01) :1-18
[8]   β-Tubulin-II Expression Strongly Predicts Outcome in Patients Receiving Induction Chemotherapy for Locally Advanced Squamous Carcinoma of the Head and Neck: A Companion Analysis of the TAX 324 Trial [J].
Cullen, Kevin J. ;
Schumaker, Lisa ;
Nikitakis, Nikolaos ;
Goloubeva, Olga ;
Tan, Ming ;
Sarlis, Nicholas J. ;
Haddad, Robert I. ;
Posner, Marshall R. .
JOURNAL OF CLINICAL ONCOLOGY, 2009, 27 (36) :6222-6228
[9]  
Cullen KJ, 2003, CANCER RES, V63, P8097
[10]  
Davis W, 2001, J PHARMACOL EXP THER, V296, P1