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Article: Roles of peroxisome proliferator-activated receptor-α and -γ in the development of non-small cell lung cancer

TitleRoles of peroxisome proliferator-activated receptor-α and -γ in the development of non-small cell lung cancer
Authors
Issue Date2010
Citation
American Journal of Respiratory Cell and Molecular Biology, 2010, v. 43 n. 6, p. 674-683 How to Cite?
AbstractPeroxisome proliferator-activated receptor Peroxisome proliferator- activated receptor (PPAR)-α and PPARδ participate in cell proliferation and apoptosis. Few studies have simultaneously investigated both PPARα and PPARγ in lung cancers in vivo. The roles of PPARα and -γ were investigated in the development of pulmonary tumors induced in the adult A/J mouse by treatment with 4-(methylnitrosamino)-l-(3-pyridyl)- lbutanone (NNK). Compared with the normal lung tissues, PPARγ expression was much higher in the NNK-induced lung tumor tissues. However, PPARγ transcriptional activity, and the levels of two major endogenous PPARγ ligands, 13-hydroxyoctadecadienoic acid and 15-hydroxyeicosatetraenoic acid, were significantly lower in the NNK-treated lung tissues. The ligand changes in mice were confirmed in human lung cancer tissues. Along with the alteration of PPARγ and its endogenous ligands, the level of PPARα and its activity were increased in the NNK-induced mouse lung tumors. Treatment of mice with the synthetic PPARγ ligand, pioglitazone, significantly inhibited the formation of mouse lung tumors induced by NNK. Our study demonstrated that the reduction of endogenous PPARγ ligands and increased PPARα occurred before the formation of lung tumors, indicating that the molecular changes play a role in lung carcinogenesis. The results suggest that the enhancement of PPARγ activity with its ligands, and the suppression of PPARα with its inhibitors, may prevent the formation of lung tumors, as well as accelerate the therapy of lung cancer. Our findings may also reveal the possibility of using the level of endogenous PPARγ ligands and the activities of PPARγ or PPARα as tumor markers for lung cancer.
Persistent Identifierhttp://hdl.handle.net/10722/192681
ISSN
2015 Impact Factor: 4.082
2015 SCImago Journal Rankings: 1.622
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLi, M-Yen_US
dc.contributor.authorYuan, Hen_US
dc.contributor.authorMa, LTen_US
dc.contributor.authorKong, AWYen_US
dc.contributor.authorHsin, MKYen_US
dc.contributor.authorYip, JHYen_US
dc.contributor.authorUnderwood, MJen_US
dc.contributor.authorChen, GGen_US
dc.date.accessioned2013-11-20T04:55:15Z-
dc.date.available2013-11-20T04:55:15Z-
dc.date.issued2010en_US
dc.identifier.citationAmerican Journal of Respiratory Cell and Molecular Biology, 2010, v. 43 n. 6, p. 674-683en_US
dc.identifier.issn1044-1549en_US
dc.identifier.urihttp://hdl.handle.net/10722/192681-
dc.description.abstractPeroxisome proliferator-activated receptor Peroxisome proliferator- activated receptor (PPAR)-α and PPARδ participate in cell proliferation and apoptosis. Few studies have simultaneously investigated both PPARα and PPARγ in lung cancers in vivo. The roles of PPARα and -γ were investigated in the development of pulmonary tumors induced in the adult A/J mouse by treatment with 4-(methylnitrosamino)-l-(3-pyridyl)- lbutanone (NNK). Compared with the normal lung tissues, PPARγ expression was much higher in the NNK-induced lung tumor tissues. However, PPARγ transcriptional activity, and the levels of two major endogenous PPARγ ligands, 13-hydroxyoctadecadienoic acid and 15-hydroxyeicosatetraenoic acid, were significantly lower in the NNK-treated lung tissues. The ligand changes in mice were confirmed in human lung cancer tissues. Along with the alteration of PPARγ and its endogenous ligands, the level of PPARα and its activity were increased in the NNK-induced mouse lung tumors. Treatment of mice with the synthetic PPARγ ligand, pioglitazone, significantly inhibited the formation of mouse lung tumors induced by NNK. Our study demonstrated that the reduction of endogenous PPARγ ligands and increased PPARα occurred before the formation of lung tumors, indicating that the molecular changes play a role in lung carcinogenesis. The results suggest that the enhancement of PPARγ activity with its ligands, and the suppression of PPARα with its inhibitors, may prevent the formation of lung tumors, as well as accelerate the therapy of lung cancer. Our findings may also reveal the possibility of using the level of endogenous PPARγ ligands and the activities of PPARγ or PPARα as tumor markers for lung cancer.en_US
dc.languageengen_US
dc.relation.ispartofAmerican Journal of Respiratory Cell and Molecular Biologyen_US
dc.titleRoles of peroxisome proliferator-activated receptor-α and -γ in the development of non-small cell lung canceren_US
dc.typeArticleen_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1165/rcmb.2009-0349OCen_US
dc.identifier.pmid20081051-
dc.identifier.scopuseid_2-s2.0-78649740044en_US
dc.identifier.volume43en_US
dc.identifier.issue6en_US
dc.identifier.spage674en_US
dc.identifier.epage683en_US
dc.identifier.isiWOS:000285013200006-

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