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Article: Elevated TAK1 augments tumor growth and metastatic capacities of ovarian cancer cells through activation of NF-κB signaling

TitleElevated TAK1 augments tumor growth and metastatic capacities of ovarian cancer cells through activation of NF-κB signaling
Authors
Issue Date2014
PublisherImpact Journals, LLC. The Journal's web site is located at http://www.impactjournals.com/oncotarget/index.html
Citation
Oncotarget, 2014, v. 5, p. 7549-7562 How to Cite?
AbstractTransforming growth factor (TGF)-β-activating kinase 1 (TAK1) is a serine/threonine kinase which is frequently associated with human cancer progression. However, its functional role in tumorigenesis is still controversial. Here, we report that TAK1 enhances the oncogenic capacity of ovarian cancer cells through the activation of NF-κB signaling. We found that TAK1 is frequently upregulated and significantly associated with high-grade and metastatic ovarian cancers. Mechanistic studies showed that Ser412 phosphorylation is required for TAK1 in activating NF-κB signaling and promotes aggressiveness of ovarian cancer cells. Conversely, suppression of TAK1 activity by point mutation at Ser412, RNAi mediated gene knockdown or TAK1 specific inhibitor ((5Z) -7-Oxozeaenol) remarkably impairs tumor growth and metastasis in ovarian cancer in vitro and in vivo. Our study underscores the importance of targeting TAK1 as a promising therapeutic approach to counteract the ovarian cancer progression.
Persistent Identifierhttp://hdl.handle.net/10722/205902
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorCAI, Cen_US
dc.contributor.authorSHI, Len_US
dc.contributor.authorLiu, VWSen_US
dc.contributor.authorTANG, WMen_US
dc.contributor.authorLIU, Jen_US
dc.contributor.authorLeung, THYen_US
dc.contributor.authorChan, KKLen_US
dc.contributor.authorYam, JWPen_US
dc.contributor.authorYao, KMen_US
dc.contributor.authorNgan, HYSen_US
dc.contributor.authorChan, DWen_US
dc.date.accessioned2014-10-20T09:26:26Z-
dc.date.available2014-10-20T09:26:26Z-
dc.date.issued2014en_US
dc.identifier.citationOncotarget, 2014, v. 5, p. 7549-7562en_US
dc.identifier.urihttp://hdl.handle.net/10722/205902-
dc.description.abstractTransforming growth factor (TGF)-β-activating kinase 1 (TAK1) is a serine/threonine kinase which is frequently associated with human cancer progression. However, its functional role in tumorigenesis is still controversial. Here, we report that TAK1 enhances the oncogenic capacity of ovarian cancer cells through the activation of NF-κB signaling. We found that TAK1 is frequently upregulated and significantly associated with high-grade and metastatic ovarian cancers. Mechanistic studies showed that Ser412 phosphorylation is required for TAK1 in activating NF-κB signaling and promotes aggressiveness of ovarian cancer cells. Conversely, suppression of TAK1 activity by point mutation at Ser412, RNAi mediated gene knockdown or TAK1 specific inhibitor ((5Z) -7-Oxozeaenol) remarkably impairs tumor growth and metastasis in ovarian cancer in vitro and in vivo. Our study underscores the importance of targeting TAK1 as a promising therapeutic approach to counteract the ovarian cancer progression.en_US
dc.languageengen_US
dc.publisherImpact Journals, LLC. The Journal's web site is located at http://www.impactjournals.com/oncotarget/index.htmlen_US
dc.relation.ispartofOncotargeten_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleElevated TAK1 augments tumor growth and metastatic capacities of ovarian cancer cells through activation of NF-κB signalingen_US
dc.typeArticleen_US
dc.identifier.emailLiu, VWS: vwsliu@hku.hken_US
dc.identifier.emailLeung, THY: thyl@hku.hken_US
dc.identifier.emailChan, KKL: kklchan@hkucc.hku.hken_US
dc.identifier.emailYam, JWP: judyyam@pathology.hku.hken_US
dc.identifier.emailYao, KM: kmyao@hku.hken_US
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_US
dc.identifier.emailChan, DW: dwchan@hku.hken_US
dc.identifier.authorityLiu, VWS=rp00341en_US
dc.identifier.authorityChan, KKL=rp00499en_US
dc.identifier.authorityYam, JWP=rp00468en_US
dc.identifier.authorityYao, KM=rp00344en_US
dc.identifier.authorityNgan, HYS=rp00346en_US
dc.identifier.authorityChan, DW=rp00543en_US
dc.description.naturepublished_or_final_version-
dc.identifier.pmcidPMC4202143-
dc.identifier.hkuros241293en_US
dc.identifier.volume5en_US
dc.identifier.spage7549en_US
dc.identifier.epage62en_US
dc.publisher.placeUSAen_US

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