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Article: 15-Lipoxygenases and its metabolites 15(S)-HETE and 13(S)-HODE in the development of non-small cell lung cancer

Title15-Lipoxygenases and its metabolites 15(S)-HETE and 13(S)-HODE in the development of non-small cell lung cancer
Authors
Issue Date2010
Citation
Thorax, 2010, v. 65 n. 4, p. 321-326 How to Cite?
AbstractBackground: 15-S-Hydroxyeicosatetraenoic acid (15(S)-HETE) and 13-S-hydroxyoctadecadienoic acid (13(S)-HODE), both of which are metabolites of 15-lipoxygenases (15-LOXs), are endogenous ligands for peroxisome proliferator-activated receptor gamma (PPARγ). The activation of PPARγ inhibits cell growth and induces apoptosis in some cancers. The role of 15(S)-HETE) and 13(S)-HODE in the development of lung cancer is not clear. Methods: 15-LOXs, 15(S)-HETE and 13(S)-HODE were monitored during the development of mouse lung tumours induced by the tobacco smoke carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and the levels of these markers were determined in 54 human non-small cell lung cancers. Results: 15-LOXs, 15(S)-HETE and 13(S)-HODE levels were significantly reduced in human lung cancer tissue compared with non-tumour lung tissue (p=0.011 and p=0.022, respectively). In mouse experiments, 15(S)-HETE and 13(S)-HODE started to reduce at 26 and 30 weeks, respectively, after NNK treatment. The time frame of 15(S)-HETE reduction was in line with the decrease in 12/15-LOX mRNA and protein. A significant difference in the number of tumours in NNK-treated mice and controls was not observed until week 34 (p<0.05) and week 38 (p<0.01). The reduction in 12/15-LOX and 15(S)-HETE therefore predated the appearance of lung tumour. Furthermore, PPARγ activity was decreased in NNK-treated mouse lungs compared with the control, and the decreased PPARγ activity occurred at the same time points as the reduction in 12/15-LOX and 15(S)-HETE. Conclusion: These findings indicate that the reduction in 15-LOX, 15(S)-HETE and 13(S)-HODE results in the decreased PPARγ activity seen in lung tumours and contributes to the development of lung tumours induced by tobacco smoking.
Persistent Identifierhttp://hdl.handle.net/10722/192676
ISSN
2015 Impact Factor: 8.121
2015 SCImago Journal Rankings: 3.650
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYuan, Hen_US
dc.contributor.authorLi, M-Yen_US
dc.contributor.authorMa, LTen_US
dc.contributor.authorHsin, MKYen_US
dc.contributor.authorMok, TSKen_US
dc.contributor.authorUnderwood, MJen_US
dc.contributor.authorChen, GGen_US
dc.date.accessioned2013-11-20T04:55:09Z-
dc.date.available2013-11-20T04:55:09Z-
dc.date.issued2010en_US
dc.identifier.citationThorax, 2010, v. 65 n. 4, p. 321-326en_US
dc.identifier.issn0040-6376en_US
dc.identifier.urihttp://hdl.handle.net/10722/192676-
dc.description.abstractBackground: 15-S-Hydroxyeicosatetraenoic acid (15(S)-HETE) and 13-S-hydroxyoctadecadienoic acid (13(S)-HODE), both of which are metabolites of 15-lipoxygenases (15-LOXs), are endogenous ligands for peroxisome proliferator-activated receptor gamma (PPARγ). The activation of PPARγ inhibits cell growth and induces apoptosis in some cancers. The role of 15(S)-HETE) and 13(S)-HODE in the development of lung cancer is not clear. Methods: 15-LOXs, 15(S)-HETE and 13(S)-HODE were monitored during the development of mouse lung tumours induced by the tobacco smoke carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and the levels of these markers were determined in 54 human non-small cell lung cancers. Results: 15-LOXs, 15(S)-HETE and 13(S)-HODE levels were significantly reduced in human lung cancer tissue compared with non-tumour lung tissue (p=0.011 and p=0.022, respectively). In mouse experiments, 15(S)-HETE and 13(S)-HODE started to reduce at 26 and 30 weeks, respectively, after NNK treatment. The time frame of 15(S)-HETE reduction was in line with the decrease in 12/15-LOX mRNA and protein. A significant difference in the number of tumours in NNK-treated mice and controls was not observed until week 34 (p<0.05) and week 38 (p<0.01). The reduction in 12/15-LOX and 15(S)-HETE therefore predated the appearance of lung tumour. Furthermore, PPARγ activity was decreased in NNK-treated mouse lungs compared with the control, and the decreased PPARγ activity occurred at the same time points as the reduction in 12/15-LOX and 15(S)-HETE. Conclusion: These findings indicate that the reduction in 15-LOX, 15(S)-HETE and 13(S)-HODE results in the decreased PPARγ activity seen in lung tumours and contributes to the development of lung tumours induced by tobacco smoking.en_US
dc.languageengen_US
dc.relation.ispartofThoraxen_US
dc.title15-Lipoxygenases and its metabolites 15(S)-HETE and 13(S)-HODE in the development of non-small cell lung canceren_US
dc.typeArticleen_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1136/thx.2009.122747en_US
dc.identifier.pmid20388757-
dc.identifier.scopuseid_2-s2.0-77950910962en_US
dc.identifier.volume65en_US
dc.identifier.issue4en_US
dc.identifier.spage321en_US
dc.identifier.epage326en_US
dc.identifier.isiWOS:000276617000010-

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