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Article: Pioglitazone prevents smoking carcinogen-induced lung tumor development in mice

TitlePioglitazone prevents smoking carcinogen-induced lung tumor development in mice
Authors
Issue Date2012
Citation
Current Cancer Drug Targets, 2012, v. 12 n. 6, p. 597-606 How to Cite?
AbstractPioglitazone (PGZ), a synthetic peroxisome proliferator-activated receptor gamma (PPARγ) ligand, is known to have anti-tumor activity by inducing tumor cell apoptosis. However, it is unknown whether it can be used to prevent smoking carcinogen-induced lung tumor development. We induced mouse lung tumors using smoking carcinogen 4- methylnitrosamino-l-3-pyridyl-butanone (NNK). PGZ was given at two early stages before the tumor formation. The role and the functional mechanism of PGZ were investigated in the development of mouse pulmonary tumors. The tumor development was monitored and PPARγ activity and endogenous PPARγ ligands 15(S)-HETE, 13(S)-HODE were determined. The application of PGZ before alveolar hyperplasia formation (Group NPa) and at the early phase of alveolar hyperplasia formation (Group NPb) significantly prevented the lung tumor development especially in Group NPb mice (all p<0.05). PGZ not only prevented the NNK-mediated reduction of endogenous ligands 15(S)-HETE and 13(S)-HODE, but also increased 13(S)-HODE level in Group NPb mice. PPARγ transcriptional activity was increased in NNKstimulated lung tissues when PGZ was given. The in vivo results were confirmed in the human lung cancer cells, which showed that PGZ induced lung cancer cell apoptosis through up-regulating nuclear PPARγ expression, inducing PPARγ transcriptional activity and increasing the levels of PPARγ ligands in NNK-treated cells. The early application of PGZ is able to prevent NNK-induced lung tumor development through maintaining the level of endogenous PPARγ ligands 15(S)-HETE and 13(S)-HODE and activation of PPARγ. © 2012 Bentham Science Publishers.
Persistent Identifierhttp://hdl.handle.net/10722/192689
ISSN
2015 Impact Factor: 3.707
2015 SCImago Journal Rankings: 1.537

 

DC FieldValueLanguage
dc.contributor.authorLi, M-Yen_US
dc.contributor.authorKong, AWYen_US
dc.contributor.authorYuan, Hen_US
dc.contributor.authorMa, LTen_US
dc.contributor.authorHsin, MKYen_US
dc.contributor.authorWan, IYPen_US
dc.contributor.authorUnderwood, MJen_US
dc.contributor.authorChen, GGen_US
dc.date.accessioned2013-11-20T04:55:21Z-
dc.date.available2013-11-20T04:55:21Z-
dc.date.issued2012en_US
dc.identifier.citationCurrent Cancer Drug Targets, 2012, v. 12 n. 6, p. 597-606en_US
dc.identifier.issn1568-0096en_US
dc.identifier.urihttp://hdl.handle.net/10722/192689-
dc.description.abstractPioglitazone (PGZ), a synthetic peroxisome proliferator-activated receptor gamma (PPARγ) ligand, is known to have anti-tumor activity by inducing tumor cell apoptosis. However, it is unknown whether it can be used to prevent smoking carcinogen-induced lung tumor development. We induced mouse lung tumors using smoking carcinogen 4- methylnitrosamino-l-3-pyridyl-butanone (NNK). PGZ was given at two early stages before the tumor formation. The role and the functional mechanism of PGZ were investigated in the development of mouse pulmonary tumors. The tumor development was monitored and PPARγ activity and endogenous PPARγ ligands 15(S)-HETE, 13(S)-HODE were determined. The application of PGZ before alveolar hyperplasia formation (Group NPa) and at the early phase of alveolar hyperplasia formation (Group NPb) significantly prevented the lung tumor development especially in Group NPb mice (all p<0.05). PGZ not only prevented the NNK-mediated reduction of endogenous ligands 15(S)-HETE and 13(S)-HODE, but also increased 13(S)-HODE level in Group NPb mice. PPARγ transcriptional activity was increased in NNKstimulated lung tissues when PGZ was given. The in vivo results were confirmed in the human lung cancer cells, which showed that PGZ induced lung cancer cell apoptosis through up-regulating nuclear PPARγ expression, inducing PPARγ transcriptional activity and increasing the levels of PPARγ ligands in NNK-treated cells. The early application of PGZ is able to prevent NNK-induced lung tumor development through maintaining the level of endogenous PPARγ ligands 15(S)-HETE and 13(S)-HODE and activation of PPARγ. © 2012 Bentham Science Publishers.en_US
dc.languageengen_US
dc.relation.ispartofCurrent Cancer Drug Targetsen_US
dc.titlePioglitazone prevents smoking carcinogen-induced lung tumor development in miceen_US
dc.typeArticleen_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.2174/156800912801784848en_US
dc.identifier.pmid22463586-
dc.identifier.scopuseid_2-s2.0-84862630157en_US
dc.identifier.volume12en_US
dc.identifier.issue6en_US
dc.identifier.spage597en_US
dc.identifier.epage606en_US

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