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Carcinogenesis Advance Access originally published online on January 20, 2005
Carcinogenesis 2005 26(4):785-791; doi:10.1093/carcin/bgi026
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Carcinogenesis vol.26 no.4 © Oxford University Press 2005; all rights reserved.

ARTICLE

Increased 5-lipoxygenase expression and induction of apoptosis by its inhibitors in esophageal cancer: a potential target for prevention

Ashraful Hoque, Scott M. Lippman, Tsung-Teh Wu1, Ya Xu, Zheng D. Liang, Stephen Swisher2, Hongfu Zhang4, Liyu Cao4, Jaffer A. Ajani3 and Xiao-chun Xu*

Departments of Clinical Cancer Prevention, 1 Pathology, 2 Thoracic and Cardiovascular Surgery and 3 Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX and 4 Department of Pathology, Anhui Medical University, Hefei, China

* To whom correspondence should be addressed. Tel: +713 745 2940; Fax: +713 563 5747; Email: xxu{at}mdanderson.org

Arachidonic acid (AA) is the major precursor of several classes of signal molecules and the alteration of its metabolism is involved in human carcinogenesis. For instance, 5-lipoxygenase (5-LOX) converts AA to hydroxyeicosatetraenoic acids or leukotrienes (LTs), which are able to enhance proliferation, increase survival and suppress the apoptosis of human cells. To determine the potential use of 5-LOX inhibitors in the prevention of esophageal cancer, we first analyzed the 5-LOX expression in esophageal tissue samples using immunohistochemistry and then examined the effect of the 5-LOX inhibitors AA861 and REV5901 on cell viability and apoptosis in esophageal cancer cell lines. 5-LOX expression was present in 79% (127/161) of esophageal cancer but in only 13% (4/32) of normal esophageal mucosa. 5-LOX was also expressed in all the eight esophageal cancer cell lines. Moreover, 5-LOX inhibitors caused a dose- and time-dependent reduction of cell viability, which was due to the induction of apoptosis and associated with LTB4 suppression. Our data also showed that both LTB4, a product of 5-LOX and LTB4 receptor antagonist U-75302 were able to prevent AA861 and REV5901 on induction of apoptosis. The present study demonstrated that 5-LOX protein expression is increased in esophageal cancer and that 5-LOX inhibitors can induce esophageal cancer cells to undergo apoptosis, suggesting that 5-LOX may be an effective target in the prevention of esophageal cancer.


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