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Conference Paper: Nuclear Met regulates liver cancer metastasis via NF-κB/MMP2 pathway

TitleNuclear Met regulates liver cancer metastasis via NF-κB/MMP2 pathway
Authors
Issue Date2016
PublisherSpringer New York LLC. The Journal's web site is located at http://www.springer.com/west/home/medicine?SGWID=4-10054-70-173733513-0
Citation
The 25th Conference of the Asian Pacific Association for the Study of the Liver (APASL 2016), Tokyo Japan, 20-24 February 2016. In Hepatology International, 2016, v. 10 n. 1 suppl., p. S282-S283, abstract no. P-0527 How to Cite?
AbstractMet is a surface receptor tyrosine kinase which upon hepatocyte growth factor induction, triggers a diversity of downstream signaling cascades that modulates different cellular processes. Emerging evidence has shown the presence of nuclear Met (nMet) in some cancerous tissues and cell lines, postulating that nMet could have unexplored functions within nucleus. Although Met is well known of its oncogenic role in hepatocellular carcinoma (HCC), existence and functions of nMet in HCC are yet to be reported. Our present study aims to examine the clinical association and functions of nMet in HCC. Immunohistochemistry of 103 human HCC paired samples showed that nMet was overexpressed in nearly 90 % of cases. We also found that nMet overexpression was progressively increased along HCC development, from non-tumorous liver tissue to early and advanced HCC. Nonetheless, nMet overexpression was significantly associated with venous invasion and poorer overall survival in HCC patients. As revealed by immunoblot and immunofluorescence, we found that nMet is about 48 kDa and comprises cytoplasmic domain of Met, as it can only be detected by an antibody against the carboxyl terminal of Met. To study the functions of nMet, we employed a lentiviral based inducible exression system to express the cytoplasmic region of Met. In vitro functional assay showed that nMet significantly promoted HCC cell proliferation and anchorage independent growth. It also significantly augmented HCC cell migration and invasiveness. Besides that, nMet also enhanced HCC tumor formation in animal model. Furthermore, we showed that nMet promoted tumor invasiveness and aggressiveness through NF-jB/MMP2 pathway.
DescriptionPoster Presentation: P-0527
This journal suppl. entitled: Abstracts of the 25th Annual Conference of APASL, February 20–24, 2016, Tokyo, Japan
Persistent Identifierhttp://hdl.handle.net/10722/229934
ISSN
2015 Impact Factor: 1.125
2015 SCImago Journal Rankings: 0.669

 

DC FieldValueLanguage
dc.contributor.authorTey, SK-
dc.contributor.authorTse, EYT-
dc.contributor.authorKo, FCF-
dc.contributor.authorMao, X-
dc.contributor.authorYam, JWP-
dc.date.accessioned2016-08-23T14:14:10Z-
dc.date.available2016-08-23T14:14:10Z-
dc.date.issued2016-
dc.identifier.citationThe 25th Conference of the Asian Pacific Association for the Study of the Liver (APASL 2016), Tokyo Japan, 20-24 February 2016. In Hepatology International, 2016, v. 10 n. 1 suppl., p. S282-S283, abstract no. P-0527-
dc.identifier.issn1936-0533-
dc.identifier.urihttp://hdl.handle.net/10722/229934-
dc.descriptionPoster Presentation: P-0527-
dc.descriptionThis journal suppl. entitled: Abstracts of the 25th Annual Conference of APASL, February 20–24, 2016, Tokyo, Japan-
dc.description.abstractMet is a surface receptor tyrosine kinase which upon hepatocyte growth factor induction, triggers a diversity of downstream signaling cascades that modulates different cellular processes. Emerging evidence has shown the presence of nuclear Met (nMet) in some cancerous tissues and cell lines, postulating that nMet could have unexplored functions within nucleus. Although Met is well known of its oncogenic role in hepatocellular carcinoma (HCC), existence and functions of nMet in HCC are yet to be reported. Our present study aims to examine the clinical association and functions of nMet in HCC. Immunohistochemistry of 103 human HCC paired samples showed that nMet was overexpressed in nearly 90 % of cases. We also found that nMet overexpression was progressively increased along HCC development, from non-tumorous liver tissue to early and advanced HCC. Nonetheless, nMet overexpression was significantly associated with venous invasion and poorer overall survival in HCC patients. As revealed by immunoblot and immunofluorescence, we found that nMet is about 48 kDa and comprises cytoplasmic domain of Met, as it can only be detected by an antibody against the carboxyl terminal of Met. To study the functions of nMet, we employed a lentiviral based inducible exression system to express the cytoplasmic region of Met. In vitro functional assay showed that nMet significantly promoted HCC cell proliferation and anchorage independent growth. It also significantly augmented HCC cell migration and invasiveness. Besides that, nMet also enhanced HCC tumor formation in animal model. Furthermore, we showed that nMet promoted tumor invasiveness and aggressiveness through NF-jB/MMP2 pathway.-
dc.languageeng-
dc.publisherSpringer New York LLC. The Journal's web site is located at http://www.springer.com/west/home/medicine?SGWID=4-10054-70-173733513-0-
dc.relation.ispartofHepatology International-
dc.rightsThe final publication is available at Springer via http://dx.doi.org/10.1007/s12072-016-9707-8-
dc.titleNuclear Met regulates liver cancer metastasis via NF-κB/MMP2 pathway-
dc.typeConference_Paper-
dc.identifier.emailTey, SK: szekeong@hku.hk-
dc.identifier.emailTse, EYT: sadietse@hkucc.hku.hk-
dc.identifier.emailKo, FCF: bokcf@hku.hk-
dc.identifier.emailMao, X: susanmao@hku.hk-
dc.identifier.emailYam, JWP: judyyam@pathology.hku.hk-
dc.identifier.authorityYam, JWP=rp00468-
dc.identifier.doi10.1007/s12072-016-9707-8-
dc.identifier.hkuros261343-
dc.identifier.volume10-
dc.identifier.issue1 suppl.-
dc.identifier.spageS282, abstract no. P-0527-
dc.identifier.epageS283-
dc.publisher.placeUnited States-

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