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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 n. 17, 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/10722/205209
ISSN
2015 Impact Factor: 5.008
2015 SCImago Journal Rankings: 2.294
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorCai, C-
dc.contributor.authorShi, L-
dc.contributor.authorLiu, VWS-
dc.contributor.authorTang, WM-
dc.contributor.authorLiu, J-
dc.contributor.authorLeung, THY-
dc.contributor.authorChan, KKL-
dc.contributor.authorYam, JWP-
dc.contributor.authorYao, KM-
dc.contributor.authorNgan, HYS-
dc.contributor.authorChan, DW-
dc.date.accessioned2014-09-20T01:59:34Z-
dc.date.available2014-09-20T01:59:34Z-
dc.date.issued2014-
dc.identifier.citationOncotarget, 2014, v. 5 n. 17, p. 7549-7562-
dc.identifier.issn1949-2553-
dc.identifier.urihttp://hdl.handle.net/10722/205209-
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.-
dc.languageeng-
dc.publisherImpact Journals LLC. The Journal's web site is located at http://www.impactjournals.com/oncotarget/index.html-
dc.relation.ispartofOncotarget-
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 signaling-
dc.typeArticle-
dc.identifier.emailShi, L: hkulshi@hku.hk-
dc.identifier.emailLiu, VWS: vwsliu@hku.hk-
dc.identifier.emailLeung, THY: thyl@hku.hk-
dc.identifier.emailChan, KKL: kklchan@hkucc.hku.hk-
dc.identifier.emailYam, JWP: judyyam@pathology.hku.hk-
dc.identifier.emailYao, KM: kmyao@hku.hk-
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hk-
dc.identifier.emailChan, DW: dwchan@hku.hk-
dc.identifier.authorityLiu, VWS=rp00341-
dc.identifier.authorityChan, KKL=rp00499-
dc.identifier.authorityYam, JWP=rp00468-
dc.identifier.authorityYao, KM=rp00344-
dc.identifier.authorityNgan, HYS=rp00346-
dc.identifier.authorityChan, DW=rp00543-
dc.description.naturepublished_or_final_version-
dc.identifier.pmcid4202143-
dc.identifier.scopuseid_2-s2.0-84907485879-
dc.identifier.hkuros236495-
dc.identifier.volume5-
dc.identifier.issue17-
dc.identifier.spage7549-
dc.identifier.epage7562-
dc.publisher.placeUnited States-

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