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Article: PPARγ activation extinguishes smoking carcinogen by inhibiting NNK-mediated proliferation

TitlePPARγ activation extinguishes smoking carcinogen by inhibiting NNK-mediated proliferation
Authors
Issue Date2010
Citation
American Journal of Respiratory Cell and Molecular Biology, 2010, v. 42 n. 1, p. 113-122 How to Cite?
AbstractAmong the carcinogenic chemicals of cigarette smoking, 4- (methylnitrosamino-1-(3-pyridyl)-1-butanone (NNK) is the most potent. The activation of peroxisome proliferator-activated receptor (PPAR)γ can arrest the growth of lung cancer. We hypothesized that PPARγ activation inhibits NNK-mediated proliferation of lung cancer cells. PPARγ expression was increased in 94.7% human lung cancer tumor tissues, compared with their paired corresponding nontumor tissues. PPARγ was also found to be abundant in all the lung cancer cell lines tested. Troglitazone dose-dependently inhibited the NNK-mediated proliferation of lung cancer cells that expressed PPARγ. Troglitazone blocked NNK-induced up-regulation of HO-1, Bcl-2, and c-IAP2, and recovered Bad activity that was suppressed by NNK. NNK promoted the nuclear p21, whereas troglitazone increased cytosolic p21. Troglitazone increased PPARγ transcriptional activity in NNK-treated cells and a PPARγ dominant-negative inhibitor completely suppressed the action of troglitazone, indicating that troglitazone against NNK was PPARγ- dependent. The findings reveal a novel molecular pathway of PPARγ activation against cigarette smoking-related lung cancer.
Persistent Identifierhttp://hdl.handle.net/10722/192672
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.authorHsin, MKYen_US
dc.contributor.authorYip, Jen_US
dc.contributor.authorMok, TSKen_US
dc.contributor.authorUnderwood, MJen_US
dc.contributor.authorChen, GGen_US
dc.date.accessioned2013-11-20T04:55:07Z-
dc.date.available2013-11-20T04:55:07Z-
dc.date.issued2010en_US
dc.identifier.citationAmerican Journal of Respiratory Cell and Molecular Biology, 2010, v. 42 n. 1, p. 113-122en_US
dc.identifier.issn1044-1549en_US
dc.identifier.urihttp://hdl.handle.net/10722/192672-
dc.description.abstractAmong the carcinogenic chemicals of cigarette smoking, 4- (methylnitrosamino-1-(3-pyridyl)-1-butanone (NNK) is the most potent. The activation of peroxisome proliferator-activated receptor (PPAR)γ can arrest the growth of lung cancer. We hypothesized that PPARγ activation inhibits NNK-mediated proliferation of lung cancer cells. PPARγ expression was increased in 94.7% human lung cancer tumor tissues, compared with their paired corresponding nontumor tissues. PPARγ was also found to be abundant in all the lung cancer cell lines tested. Troglitazone dose-dependently inhibited the NNK-mediated proliferation of lung cancer cells that expressed PPARγ. Troglitazone blocked NNK-induced up-regulation of HO-1, Bcl-2, and c-IAP2, and recovered Bad activity that was suppressed by NNK. NNK promoted the nuclear p21, whereas troglitazone increased cytosolic p21. Troglitazone increased PPARγ transcriptional activity in NNK-treated cells and a PPARγ dominant-negative inhibitor completely suppressed the action of troglitazone, indicating that troglitazone against NNK was PPARγ- dependent. The findings reveal a novel molecular pathway of PPARγ activation against cigarette smoking-related lung cancer.en_US
dc.languageengen_US
dc.relation.ispartofAmerican Journal of Respiratory Cell and Molecular Biologyen_US
dc.titlePPARγ activation extinguishes smoking carcinogen by inhibiting NNK-mediated proliferationen_US
dc.typeArticleen_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1165/rcmb.2008-0463OCen_US
dc.identifier.pmid19346318-
dc.identifier.scopuseid_2-s2.0-73949133483en_US
dc.identifier.volume42en_US
dc.identifier.issue1en_US
dc.identifier.spage113en_US
dc.identifier.epage122en_US
dc.identifier.isiWOS:000273204500015-

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