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Carcinogenesis Advance Access originally published online on May 19, 2006
Carcinogenesis 2006 27(11):2308-2315; doi:10.1093/carcin/bgl073
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Alpha-tocopheryl succinate, in contrast to alpha-tocopherol and alpha-tocopheryl acetate, inhibits prostaglandin E2 production in human lung epithelial cells

Eunmyong Lee1,2, Moon-Kyung Choi2, Young-Ju Lee2, Ja-Lok Ku3, Kyung-Hee Kim3, Jin-Sung Choi3 and Soo-Jeong Lim1,2,*

1 Department of Bioscience and Biotechnology, Sejong University Seoul, Korea
2 Research Institute, National Cancer Center Goyang, Gyeonggi, Korea
3 Laboratory of Cell Biology, Cancer Research Center and Cancer Research Institute, Seoul National University College of Medicine Seoul, Korea

*To whom correspondence should be addressed at: Department of Bioscience and Biotechnology, Sejong University, 98 Kunja-dong, Kwangjin-gu, Seoul 143-747, Korea. Tel: +82 2 3408 3334; Fax: +82 2 3408 3334; Email: sjlim61{at}hotmail.com

The production of prostaglandin E2 (PGE2), a key proinflammatory mediator, is regulated by the availability of its substrate, arachidonic acid (AA), and the activity of the enzyme cyclooxygenase (COX). Increased PGE2 production and COX-2 expression have been observed frequently in specimens from lung cancer patients. Agents that decrease PGE2 production may prevent the initiation and progression of lung cancer. We, therefore, tested the effects of alpha-tocopherol ({alpha}TOL) analogs on PGE2 production in human lung epithelial cells. Alpha-tocopheryl succinate ({alpha}TOS), but not {alpha}TOL or alpha-tocopheryl acetate ({alpha}TOA), inhibited the phorbol 12-myristate 13-acetate (PMA)-stimulated PGE2 production in three human lung epithelial cell lines (BEAS-2B, H460 and A549 cells). The effect of these compounds on PGE2 production was not correlated with their antioxidant activities, since {alpha}TOS alone did not inhibit PMA-induced generation of reactive oxygen species. {alpha}TOS had no effect on PMA-induced AA release or COX-2 expression, although post-incubation with {alpha}TOS inhibited COX activity and prostaglandin (PGE2 and PGF2{alpha}) production in PMA-stimulated cells. {alpha}TOS also blocked the COX activity in A549 cells with endogenous high levels of COX enzymes in the absence of PMA stimulation. In addition, the ability of {alpha}TOS to inhibit COX was affected by AA concentration, suggesting that {alpha}TOS may compete with AA for interaction with COX proteins. These results suggest that {alpha}TOS inhibits COX activity, thereby inhibiting PGE2 production in human lung epithelial cells, despite the lack of antioxidant activity. Administration of {alpha}TOS may block inflammatory responses mediated by PGE2, thereby inhibiting the initiation and progression of lung cancer.


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