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Article: Nuclear Met promotes hepatocellular carcinoma tumorigenesis and metastasis by upregulation of TAK1 and activation of NF-κB pathway

TitleNuclear Met promotes hepatocellular carcinoma tumorigenesis and metastasis by upregulation of TAK1 and activation of NF-κB pathway
Authors
KeywordsHepatocellular carcinoma
Metastasis
Nuclear Met
Nuclear factor kappa B
Transforming growth factor beta-activated kinase 1
Issue Date2017
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2017, v. 411, p. 150-161 How to Cite?
AbstractPresence of Met receptor tyrosine kinase in the nucleus of cells has been reported. However, the functions of Met which expresses in the nucleus (nMet) remain elusive. In this study, we found that nMet was increased in 89% of HCC tumorous tissues when compared with the corresponding non-tumorous liver tissues. nMet expression increased progressively along HCC development and significantly correlated with cirrhosis, poorer cellular differentiation, venous invasion, late stage HCC and poorer overall survival. Western blot analysis revealed that nMet is a 48-kDa protein comprising the carboxyl terminal of Met receptor. Induced expression of nMet promoted HCC cell growth, migration and invasiveness in vitro and tumorigenesis and pulmonary metastasis in vivo. Luciferase assay showed that nMet activated NF-κB pathway. Indeed, p-IKKα/β and nuclear p-p65 were higher in nMet stable cells than in the control cells. Perturbation of TAK1/NF-κB axis abrogated the aggressiveness of HCC cells, both in vitro and in vivo. In conclusion, nMet was overexpressed and as a potential prognostic biomarker of HCC. Functionally, nMet accelerated HCC tumorigenesis and metastasis via the activation of TAK1/NF-κB pathway.
Persistent Identifierhttp://hdl.handle.net/10722/254894
ISSN
2015 Impact Factor: 5.992
2015 SCImago Journal Rankings: 2.331

 

DC FieldValueLanguage
dc.contributor.authorTey, SK-
dc.contributor.authorTse, EYT-
dc.contributor.authorMao, X-
dc.contributor.authorKo, FCF-
dc.contributor.authorWong, AST-
dc.contributor.authorLo, CLR-
dc.contributor.authorNg, IOL-
dc.contributor.authorYam, JWP-
dc.date.accessioned2018-06-21T01:08:15Z-
dc.date.available2018-06-21T01:08:15Z-
dc.date.issued2017-
dc.identifier.citationCancer Letters, 2017, v. 411, p. 150-161-
dc.identifier.issn0304-3835-
dc.identifier.urihttp://hdl.handle.net/10722/254894-
dc.description.abstractPresence of Met receptor tyrosine kinase in the nucleus of cells has been reported. However, the functions of Met which expresses in the nucleus (nMet) remain elusive. In this study, we found that nMet was increased in 89% of HCC tumorous tissues when compared with the corresponding non-tumorous liver tissues. nMet expression increased progressively along HCC development and significantly correlated with cirrhosis, poorer cellular differentiation, venous invasion, late stage HCC and poorer overall survival. Western blot analysis revealed that nMet is a 48-kDa protein comprising the carboxyl terminal of Met receptor. Induced expression of nMet promoted HCC cell growth, migration and invasiveness in vitro and tumorigenesis and pulmonary metastasis in vivo. Luciferase assay showed that nMet activated NF-κB pathway. Indeed, p-IKKα/β and nuclear p-p65 were higher in nMet stable cells than in the control cells. Perturbation of TAK1/NF-κB axis abrogated the aggressiveness of HCC cells, both in vitro and in vivo. In conclusion, nMet was overexpressed and as a potential prognostic biomarker of HCC. Functionally, nMet accelerated HCC tumorigenesis and metastasis via the activation of TAK1/NF-κB pathway.-
dc.languageeng-
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet-
dc.relation.ispartofCancer Letters-
dc.subjectHepatocellular carcinoma-
dc.subjectMetastasis-
dc.subjectNuclear Met-
dc.subjectNuclear factor kappa B-
dc.subjectTransforming growth factor beta-activated kinase 1-
dc.titleNuclear Met promotes hepatocellular carcinoma tumorigenesis and metastasis by upregulation of TAK1 and activation of NF-κB pathway-
dc.typeArticle-
dc.identifier.emailWong, AST: awong1@hku.hk-
dc.identifier.emailLo, CLR: loregina@hku.hk-
dc.identifier.emailNg, IOL: iolng@hku.hk-
dc.identifier.emailYam, JWP: jywp@hkucc.hku.hk-
dc.identifier.authorityWong, AST=rp00805-
dc.identifier.authorityLo, CLR=rp01359-
dc.identifier.authorityNg, IOL=rp00335-
dc.identifier.authorityYam, JWP=rp00468-
dc.identifier.doi10.1016/j.canlet.2017.09.047-
dc.identifier.pmid28989054-
dc.identifier.hkuros285477-
dc.identifier.hkuros286532-
dc.identifier.volume411-
dc.identifier.spage150-
dc.identifier.epage161-
dc.publisher.placeIreland-

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