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Article: Contributory role of 5-lipoxygenase and its association with angiogenesis in the promotion of inflammation-associated colonic tumorigenesis by cigarette smoking

TitleContributory role of 5-lipoxygenase and its association with angiogenesis in the promotion of inflammation-associated colonic tumorigenesis by cigarette smoking
Authors
KeywordsCigarette smoking
Angiogenesis
5-Lipoxygenase
Dextran sulfate sodium
Colon cancer
Issue Date2004
Citation
Toxicology, 2004, v. 203, n. 1-3, p. 179-188 How to Cite?
AbstractOur previous study shows that cigarette smoking can promote inflammation-associated adenoma formation in the mouse colon, but the underling mechanism remains unknown. Several studies suggest that there is a link between 5-lipoxygenase (5-LOX) and carcinogenesis in humans and animals. In the present study, we aims to investigate whether the promoting action of cigarette smoke on inflammation-associated colon cancer formation is associated with 5-LOX activation in mice. Results showed that exposure to the mainstream smoke of unfiltered cigarettes enhanced the 5-LOX protein expression in the inflammation-associated colonic adenomas. It was accompanied with an up-regulation of matrix metalloproteinase-2 (MMP-2) and vascular endothelial growth factor (VEGF). Both are the key angiogenic factors for tumorigenesis. 5-LOX inhibitors decreased the incidence of colonic adenoma formation and reduced angiogenesis, MMP-2 activity and VEGF protein expression in the colons of these animals. Taken together, these results strongly suggest that cigarette smoke can induce 5-LOX expression which plays an important role in activation of MMP-2 and VEGF to induce angiogenic process and promotion of inflammation-associated adenoma formation in mice. © 2004 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/207511
ISSN
2015 Impact Factor: 3.817
2015 SCImago Journal Rankings: 1.335

 

DC FieldValueLanguage
dc.contributor.authorYe, Yini-
dc.contributor.authorLiu, Edgar Shiu Lam-
dc.contributor.authorShin, Vivianyvonne-
dc.contributor.authorWu, William Ka Kei-
dc.contributor.authorCho, Chihin-
dc.date.accessioned2014-12-31T01:01:48Z-
dc.date.available2014-12-31T01:01:48Z-
dc.date.issued2004-
dc.identifier.citationToxicology, 2004, v. 203, n. 1-3, p. 179-188-
dc.identifier.issn0300-483X-
dc.identifier.urihttp://hdl.handle.net/10722/207511-
dc.description.abstractOur previous study shows that cigarette smoking can promote inflammation-associated adenoma formation in the mouse colon, but the underling mechanism remains unknown. Several studies suggest that there is a link between 5-lipoxygenase (5-LOX) and carcinogenesis in humans and animals. In the present study, we aims to investigate whether the promoting action of cigarette smoke on inflammation-associated colon cancer formation is associated with 5-LOX activation in mice. Results showed that exposure to the mainstream smoke of unfiltered cigarettes enhanced the 5-LOX protein expression in the inflammation-associated colonic adenomas. It was accompanied with an up-regulation of matrix metalloproteinase-2 (MMP-2) and vascular endothelial growth factor (VEGF). Both are the key angiogenic factors for tumorigenesis. 5-LOX inhibitors decreased the incidence of colonic adenoma formation and reduced angiogenesis, MMP-2 activity and VEGF protein expression in the colons of these animals. Taken together, these results strongly suggest that cigarette smoke can induce 5-LOX expression which plays an important role in activation of MMP-2 and VEGF to induce angiogenic process and promotion of inflammation-associated adenoma formation in mice. © 2004 Elsevier Ireland Ltd. All rights reserved.-
dc.languageeng-
dc.relation.ispartofToxicology-
dc.subjectCigarette smoking-
dc.subjectAngiogenesis-
dc.subject5-Lipoxygenase-
dc.subjectDextran sulfate sodium-
dc.subjectColon cancer-
dc.titleContributory role of 5-lipoxygenase and its association with angiogenesis in the promotion of inflammation-associated colonic tumorigenesis by cigarette smoking-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.tox.2004.06.004-
dc.identifier.pmid15363593-
dc.identifier.scopuseid_2-s2.0-4444354992-
dc.identifier.volume203-
dc.identifier.issue1-3-
dc.identifier.spage179-
dc.identifier.epage188-

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