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Article: Thromboxane synthase suppression induces lung cancer cell apoptosis via inhibiting NF-κB

TitleThromboxane synthase suppression induces lung cancer cell apoptosis via inhibiting NF-κB
Authors
Issue Date2010
Citation
Experimental Cell Research, 2010, v. 316 n. 20, p. 3468-3477 How to Cite?
AbstractAccumulating evidence shows that the inhibition of thromboxane synthase (TXS) induced apoptosis in cancer cells. TXS inhibitor 1-Benzylimidzole (1-BI) can trigger apoptosis in lung cancer cells but the mechanism is not fully defined. In this study, lung cancer cells were treated with 1-BI. In this study, the level of reactive oxygen species (ROS) was measured and NF-κB activity was determined in human lung cancer cells. The roles of ROS and NF-κB in 1-BI-mediated cell death were analyzed. The results showed that 1-BI induced ROS generation but decreased the activity of NF-κB by reducing phosphorylated IκBα (p-IκBα) and inhibiting the translocation of p65 into the nucleus. In contrast to 1-BI, antioxidant N-acetyl cysteine (NAC) stimulated cell proliferation and significantly protected the cells from 1-BI-mediated cell death by neutralizing ROS. Collectively, apoptosis induced by 1-BI is associated with the over-production of ROS and the reduction of NF-κB. Antioxidants can significantly block the inhibitory effect of 1-BI. © 2010 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/192680
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.authorLi, M-Yen_US
dc.contributor.authorLeung, BCSen_US
dc.contributor.authorHsin, MKYen_US
dc.contributor.authorMok, TSKen_US
dc.contributor.authorUnderwood, MJen_US
dc.contributor.authorChen, GGen_US
dc.date.accessioned2013-11-20T04:55:14Z-
dc.date.available2013-11-20T04:55:14Z-
dc.date.issued2010en_US
dc.identifier.citationExperimental Cell Research, 2010, v. 316 n. 20, p. 3468-3477en_US
dc.identifier.issn0014-4827en_US
dc.identifier.urihttp://hdl.handle.net/10722/192680-
dc.description.abstractAccumulating evidence shows that the inhibition of thromboxane synthase (TXS) induced apoptosis in cancer cells. TXS inhibitor 1-Benzylimidzole (1-BI) can trigger apoptosis in lung cancer cells but the mechanism is not fully defined. In this study, lung cancer cells were treated with 1-BI. In this study, the level of reactive oxygen species (ROS) was measured and NF-κB activity was determined in human lung cancer cells. The roles of ROS and NF-κB in 1-BI-mediated cell death were analyzed. The results showed that 1-BI induced ROS generation but decreased the activity of NF-κB by reducing phosphorylated IκBα (p-IκBα) and inhibiting the translocation of p65 into the nucleus. In contrast to 1-BI, antioxidant N-acetyl cysteine (NAC) stimulated cell proliferation and significantly protected the cells from 1-BI-mediated cell death by neutralizing ROS. Collectively, apoptosis induced by 1-BI is associated with the over-production of ROS and the reduction of NF-κB. Antioxidants can significantly block the inhibitory effect of 1-BI. © 2010 Elsevier Inc.en_US
dc.languageengen_US
dc.relation.ispartofExperimental Cell Researchen_US
dc.titleThromboxane synthase suppression induces lung cancer cell apoptosis via inhibiting NF-κBen_US
dc.typeArticleen_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.yexcr.2010.07.003en_US
dc.identifier.pmid20647010-
dc.identifier.scopuseid_2-s2.0-78149415410en_US
dc.identifier.volume316en_US
dc.identifier.issue20en_US
dc.identifier.spage3468en_US
dc.identifier.epage3477en_US
dc.identifier.isiWOS:000284523600015-

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