File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Conference Paper: In vitro growth inhibitory effects of arsenic trioxide in non-small cell lung cancer with different K-ras mutations

TitleIn vitro growth inhibitory effects of arsenic trioxide in non-small cell lung cancer with different K-ras mutations
Authors
KeywordsBiology
Biochemistry
Issue Date2010
PublisherWiley-Blackwell Publishing Ltd..
Citation
The 35th Congress of the Federation of European Biochemical Societies (FEBS 2010), Gothenburg, Sweden, 26 June-1 July 2010. In The FEBS Journal, 2010, v. 277 suppl. S1, p. 136, abstract no. B2.61 How to Cite?
AbstractK-Ras mutation is frequently related to resistance of tyrosine kinase inhibitor (TKI) therapy for non-small cell lung cancer (NSCLC). Arsenic trioxide (ATO), as a novel anticancer drug, is primarily used to cure acute promyolocytic leukemia. However, for other types of cancers the effects of ATO are still unveiled. Here we test in vitro growth inhibitory effects of ATO in two NSCLC cell lines: H23 (K-Ras mutant) and HCC827 (K-Ras wild type) in hope of shedding light on overcoming the de novo resistance resulted by TKI treatments. ATO induces more cell death compared to Erlotinib (one small-molecule TKI in clinical use) as well as cell apoptosis. ATO leads to down-regulations of both phosphor-Akt and Akt while Erlotinib just diminishes phosphor-Akt. Of the Ras/Raf/Erk pathway, ATO enhances the phosphorylation of Erk1/2 significantly in H23 but not in HCC827. In order to prove that downstream signalings following activation of Erk1/2 are driven to apoptosis instead of cell proliferation in H23, we examined the change of Bax which is believed to play an important role at intrinsic apoptosis. Surprisingly, Bax is down-regulated in a dose- and time-dependent manner. Before the further explorations of this phenomenon, current acceptable explanation would be either that ATO is working through extrinsic apoptotic pathways or that ATO effects diversified signaling which combined together lead to final apoptosis at K-Ras mutant cell lines of NSCLC.
DescriptionConference Theme: Molecules of Life
Symposium B - Molecular Networks: B2 - Signal Transduction (Poster Presentation)
Persistent Identifierhttp://hdl.handle.net/10722/137777
ISSN

 

DC FieldValueLanguage
dc.contributor.authorHe, Fen_US
dc.contributor.authorKwong, YLen_US
dc.contributor.authorHo, CMen_US
dc.date.accessioned2011-08-26T14:33:14Z-
dc.date.available2011-08-26T14:33:14Z-
dc.date.issued2010en_US
dc.identifier.citationThe 35th Congress of the Federation of European Biochemical Societies (FEBS 2010), Gothenburg, Sweden, 26 June-1 July 2010. In The FEBS Journal, 2010, v. 277 suppl. S1, p. 136, abstract no. B2.61en_US
dc.identifier.issn1742-4658-
dc.identifier.urihttp://hdl.handle.net/10722/137777-
dc.descriptionConference Theme: Molecules of Life-
dc.descriptionSymposium B - Molecular Networks: B2 - Signal Transduction (Poster Presentation)-
dc.description.abstractK-Ras mutation is frequently related to resistance of tyrosine kinase inhibitor (TKI) therapy for non-small cell lung cancer (NSCLC). Arsenic trioxide (ATO), as a novel anticancer drug, is primarily used to cure acute promyolocytic leukemia. However, for other types of cancers the effects of ATO are still unveiled. Here we test in vitro growth inhibitory effects of ATO in two NSCLC cell lines: H23 (K-Ras mutant) and HCC827 (K-Ras wild type) in hope of shedding light on overcoming the de novo resistance resulted by TKI treatments. ATO induces more cell death compared to Erlotinib (one small-molecule TKI in clinical use) as well as cell apoptosis. ATO leads to down-regulations of both phosphor-Akt and Akt while Erlotinib just diminishes phosphor-Akt. Of the Ras/Raf/Erk pathway, ATO enhances the phosphorylation of Erk1/2 significantly in H23 but not in HCC827. In order to prove that downstream signalings following activation of Erk1/2 are driven to apoptosis instead of cell proliferation in H23, we examined the change of Bax which is believed to play an important role at intrinsic apoptosis. Surprisingly, Bax is down-regulated in a dose- and time-dependent manner. Before the further explorations of this phenomenon, current acceptable explanation would be either that ATO is working through extrinsic apoptotic pathways or that ATO effects diversified signaling which combined together lead to final apoptosis at K-Ras mutant cell lines of NSCLC.-
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing Ltd..-
dc.relation.ispartofThe FEBS Journalen_US
dc.rightsThe definitive version is available at www3.interscience.wiley.com-
dc.subjectBiology-
dc.subjectBiochemistry-
dc.titleIn vitro growth inhibitory effects of arsenic trioxide in non-small cell lung cancer with different K-ras mutationsen_US
dc.typeConference_Paperen_US
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1742-4658&volume=277 &issue=Suppl, s1&spage=136, abstract no. B2.61&epage=&date=2010&atitle=In+vitro+growth+inhibitory+effects+of+arsenic+trioxide+in+non-small+cell+lung+cancer+with+different+K-ras+mutations-
dc.identifier.emailKwong, YL: ylkwong@hku.hken_US
dc.identifier.emailHo, CM: jhocm@hku.hken_US
dc.identifier.authorityKwong, YL=rp00358en_US
dc.identifier.authorityHo, CM=rp00258en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1111/j.1742-4658.2010.07680.x-
dc.identifier.hkuros190415en_US
dc.identifier.volume277en_US
dc.identifier.issuesuppl. S1en_US
dc.identifier.spage136, abstract no. B2.61en_US
dc.identifier.epage136, abstract no. B2.61en_US
dc.publisher.placeUnited Kingdom-
dc.description.otherThe 35th FEBS (Federation of European Biochemical Societies) Congress, Gothenburg, Sweden, 26 June-1 July 2010. In The FEBS Journal, 2010, v. 277 suppl. s1, p. 136, abstract no. B2.61-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats