Dietary tocopherols inhibit cell proliferation, regulate expression of ER, PPAR, and Nrf2, and decrease serum inflammatory markers during the development of mammary hyperplasia
- Authors
- Smolarek, Amanda K.; So, Jae Young; Thomas, Paul E.; Lee, Hong Jin; Paul, Shiby; Dombrowski, Anne; Wang, Chung-Xiou; Saw, Constance Lay-Lay; Khor, Tin Oo; Kong, Ah-Ng Tony; Reuhl, Kenneth; Lee, Mao-Jung; Yang, Chung S.; Suh, Nanjoo
- Issue Date
- Jul-2013
- Publisher
- WILEY
- Keywords
- vitamin E; tocopherol; breast cancer; estrogen receptor; peroxisome proliferator-activated receptor
- Citation
- MOLECULAR CARCINOGENESIS, v.52, no.7, pp 514 - 525
- Pages
- 12
- Journal Title
- MOLECULAR CARCINOGENESIS
- Volume
- 52
- Number
- 7
- Start Page
- 514
- End Page
- 525
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/14493
- DOI
- 10.1002/mc.21886
- ISSN
- 0899-1987
1098-2744
- Abstract
- Previous clinical and epidemiological studies of vitamin E have used primarily -tocopherol for the prevention of cancer. However, -tocopherol has demonstrated greater anti-inflammatory and anti-tumor activity than -tocopherol in several animal models of cancer. This study assessed the potential chemopreventive activities of a tocopherol mixture containing 58% -tocopherol (-TmT) in an established rodent model of mammary carcinogenesis. Female ACI rats were utilized due to their sensitivity to 17-estradiol (E2) to induce mammary hyperplasia and neoplasia. The rats were implanted subcutaneously with sustained release E2 pellets and given dietary 0.3% or 0.5% -TmT for 2 or 10wk. Serum E2 levels were significantly reduced by the treatment with 0.5% -TmT. Serum levels of inflammatory markers, prostaglandin E2 and 8-isoprostane, were suppressed by -TmT treatment. Histology of mammary glands showed evidence of epithelial hyperplasia in E2-treated rats. Immunohistochemical analysis of the mammary glands revealed a decrease in proliferating cell nuclear antigen (PCNA), cyclooxygenase-2 (COX-2), and estrogen receptor (ER), while there was an increase in cleaved-caspase 3, peroxisome proliferator-activated receptor (PPAR), and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) in -TmT-treated rats. In addition, treatment with -TmT resulted in a decrease in the expression of ER mRNA, whereas mRNA levels of ER and PPAR were increased. In conclusion, -TmT was shown to suppress inflammatory markers, inhibit E2-induced cell proliferation, and upregulate PPAR and Nrf2 expression in mammary hyperplasia, suggesting that -TmT may be a promising agent for human breast cancer prevention. (c) 2012 Wiley Periodicals, Inc.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - ETC > 1. Journal Articles
![qrcode](https://api.qrserver.com/v1/create-qr-code/?size=55x55&data=https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/14493)
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.