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Article: Inhibition of thromboxane synthase induces lung cancer cell death via increasing the nuclear p27

TitleInhibition of thromboxane synthase induces lung cancer cell death via increasing the nuclear p27
Authors
Issue Date2009
Citation
Experimental Cell Research, 2009, v. 315 n. 17, p. 2974-2981 How to Cite?
AbstractThe role of thromboxane in lung carcinogenesis is not clearly known, though thromboxane B2 (TXB 2) level is increased and antagonists of thromboxane receptors or TXA2 can induce apoptosis of lung cancer cells. p27, an atypical tumor suppressor, is normally sequestered in the nucleus. The increased nuclear p27 may result in apoptosis of tumor cells. We hypothesize that the inhibition of thromboxane synthase (TXS) induces the death of lung cancer cells and that such inhibition is associated with the nuclear p27 level. Our experiment showed that the inhibition of TXS significantly induced the death or apoptosis in lung cancer cells. The activity of TXS was increased in lung cancer. The nuclear p27 was remarkably reduced in lung cancer tissues. The inhibition of TXS caused the cell death and apoptosis of lung cancer cells, likely via the elevation of the nuclear p27 since the TXS inhibition promoted the nuclear p27 level and the inhibition of p27 by its siRNA recovered the cell death induced by TXS inhibition. Collectively, lung cancer cells produce high levels of TXB 2 but their nuclear p27 is markedly reduced. The inhibition of TXS results in the p27-related induction of cell death in lung cancer cells. © 2009 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/192670
ISSN
2015 Impact Factor: 3.378
2015 SCImago Journal Rankings: 1.900
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLeung, KCen_US
dc.contributor.authorHsin, MKYen_US
dc.contributor.authorChan, JSYen_US
dc.contributor.authorYip, JHYen_US
dc.contributor.authorLi, Men_US
dc.contributor.authorLeung, BCSen_US
dc.contributor.authorMok, TSKen_US
dc.contributor.authorWarner, TDen_US
dc.contributor.authorUnderwood, MJen_US
dc.contributor.authorChen, GGen_US
dc.date.accessioned2013-11-20T04:55:05Z-
dc.date.available2013-11-20T04:55:05Z-
dc.date.issued2009en_US
dc.identifier.citationExperimental Cell Research, 2009, v. 315 n. 17, p. 2974-2981en_US
dc.identifier.issn0014-4827en_US
dc.identifier.urihttp://hdl.handle.net/10722/192670-
dc.description.abstractThe role of thromboxane in lung carcinogenesis is not clearly known, though thromboxane B2 (TXB 2) level is increased and antagonists of thromboxane receptors or TXA2 can induce apoptosis of lung cancer cells. p27, an atypical tumor suppressor, is normally sequestered in the nucleus. The increased nuclear p27 may result in apoptosis of tumor cells. We hypothesize that the inhibition of thromboxane synthase (TXS) induces the death of lung cancer cells and that such inhibition is associated with the nuclear p27 level. Our experiment showed that the inhibition of TXS significantly induced the death or apoptosis in lung cancer cells. The activity of TXS was increased in lung cancer. The nuclear p27 was remarkably reduced in lung cancer tissues. The inhibition of TXS caused the cell death and apoptosis of lung cancer cells, likely via the elevation of the nuclear p27 since the TXS inhibition promoted the nuclear p27 level and the inhibition of p27 by its siRNA recovered the cell death induced by TXS inhibition. Collectively, lung cancer cells produce high levels of TXB 2 but their nuclear p27 is markedly reduced. The inhibition of TXS results in the p27-related induction of cell death in lung cancer cells. © 2009 Elsevier Inc. All rights reserved.en_US
dc.languageengen_US
dc.relation.ispartofExperimental Cell Researchen_US
dc.titleInhibition of thromboxane synthase induces lung cancer cell death via increasing the nuclear p27en_US
dc.typeArticleen_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.yexcr.2009.06.025en_US
dc.identifier.pmid19576211-
dc.identifier.scopuseid_2-s2.0-70349439120en_US
dc.identifier.volume315en_US
dc.identifier.issue17en_US
dc.identifier.spage2974en_US
dc.identifier.epage2981en_US
dc.identifier.isiWOS:000270739600011-

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