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Oxidative Medicine and Cellular Longevity
Volume 2014 (2014), Article ID 787195, 9 pages
Research Article

Promoter Hypermethylation and Suppression of Glutathione Peroxidase 3 Are Associated with Inflammatory Breast Carcinogenesis

1Department of Zoology, Faculty of Science, Cairo University, Giza 12613, Egypt
2Department of Surgery, Vanderbilt University Medical Center, Nashville, TN 37232, USA
3Department of Pathology, National Cancer Institute, Cairo University, Giza 12613, Egypt
4Department of General Surgery, Faculty of Medicine, Ain Shams University, Cairo 11566, Egypt

Received 25 November 2013; Revised 22 January 2014; Accepted 30 January 2014; Published 20 March 2014

Academic Editor: Jeannette Vasquez-Vivar

Copyright © 2014 Mona M. Mohamed et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Reactive oxygen species (ROS) play a crucial role in breast cancer initiation, promotion, and progression. Inhibition of antioxidant enzymes that remove ROS was found to accelerate cancer growth. Studies showed that inhibition of glutathione peroxidase-3 (GPX3) was associated with cancer progression. Although the role of GPX3 has been studied in different cancer types, its role in breast cancer and its epigenetic regulation have not yet been investigated. The aim of the present study was to investigate GPX3 expression and epigenetic regulation in carcinoma tissues of breast cancer patients’ in comparison to normal breast tissues. Furthermore, we compared GPX3 level of expression and methylation status in aggressive phenotype inflammatory breast cancer (IBC) versus non-IBC invasive ductal carcinoma (IDC). We found that GPX3 mRNA and protein expression levels were downregulated in the carcinoma tissues of IBC compared to non-IBC. However, we did not detect significant correlation between GPX3 and patients’ clinical-pathological prosperities. Promoter hypermethylation of GPX3 gene was detected in carcinoma tissues not normal breast tissues. In addition, IBC carcinoma tissues showed a significant increase in the promoter hypermethylation of GPX3 gene compared to non-IBC. Our results propose that downregulation of GPX3 in IBC may play a role in the disease progression.