buy adobe photoshop 7.0 1 cost of camtasia studio price of ms office trial best price photoshop elements 8.0 purchase access 2003 upgrade buy autodesk inventor online discount dragon naturallyspeaking 10 buy apple aperture 2.0 software purchase outlook for mac separately best buy adobe premiere elements 8 purchase adobe dreamweaver cs5 buy outlook 2010 uk buy windows xp cd key online buy paperport 11 software cheapest office 2010
buy autocad 2009 lt uk access 2010 best price buy microsoft works 9.0 online can you buy windows 7 starter edition buy wordperfect office 2000 purchase adobe photoshop cs3 upgrade microsoft word for mac purchase price of solidworks 2009 buying windows 7 server buy ableton live 8 cheapest adobe acrobat 9 standard purchase dreamweaver 8 software purchase adobe photoshop cs3 extended purchase dragon naturally speaking 11 cheap windows 7 product key

Ethanol Promotes Chemically Induced Oral Cancer in Mice through Activation of the 5-Lipoxygenase Pathway of Arachidonic Acid Metabolism

Wed, Oct 19, 2011

Oral Cancer News

Source: Cancer Prevention Research

Abstract

Alcohol drinking is a known risk factor for oral cancer in humans. However, previous animal studies on the promoting effect of ethanol on oral carcinogenesis were inconclusive. It is necessary to develop an animal model with which the molecular mechanism of ethanol-related oral carcinogenesis may be elucidated to develop effective prevention strategies. In this study, mice were first treated with 4-nitroquinoline-1-oxide (4NQO, 100 μg/mL in drinking water) for 8 weeks and then given water or ethanol (8%) as the sole drink for another 16 weeks. During the experiment, 8% ethanol was well tolerated by mice. The incidence of squamous cell carcinoma (SCC) increased from 20% (8/41) to 43% (17/40; P < 0.05). Expression of 5-lipoxygenase (5-Lox) and cyclooxygenase 2 (Cox-2) was increased in dysplasia and SCC of 4NQO-treated tongues and further enhanced by ethanol. Using this mouse model, we further showed that fewer cancers were induced in Alox5−/− mice, as were cell proliferation, inflammation, and angiogenesis in the tongue, as compared with Alox5+/+ mice. Interestingly, Cox-2 expression was induced by ethanol in knockout mice, whereas 5-Lox and leukotriene A4 hydrolase (LTA4H) expression and leukotriene B4 (LTB4) biosynthesis were dramatically reduced. Moreover, ethanol enhanced expression and nuclear localization of 5-Lox and stimulated LTB4 biosynthesis in human tongue SCC cells (SCC-15 and SCC-4) in vitro. In conclusion, this study clearly showed that ethanol promoted 4NQO-induced oral carcinogenesis, at least in part, through further activation of the 5-Lox pathway of arachidonic acid metabolism.

This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.

Print Friendly
Be Sociable, Share!
, , , ,

Leave a Reply

You must be logged in to post a comment.