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Conference Paper: Overexpression of PAK4 in hepatocellular carcinoma (HCC)

TitleOverexpression of PAK4 in hepatocellular carcinoma (HCC)
Authors
Issue Date2006
PublisherAmerican Association for Cancer Research.
Citation
The 97th Annual Meeting of the American Association for Cancer Research (AACR 2006), Washington, DC., 1-5 April 2006. In Cancer Research, 2006, v. 66 n. 8S, p. 1204, abstract no. 5133 How to Cite?
Abstractp21-activated protein kinases (PAKs) are activated by the small Rho family GTPases, Cdc42 and Rac1, in response to various extracellular signals and act in a variety of cellular processes including cell proliferation, morphology, motility, death and survival. PAK-4 is a newly identified Group II member of the PAK family. Like the Group I PAKs, PAK-4 contains an N-terminal p21 binding domain (PBD) and a C-terminal kinase domain, but lacks the auto-inhibitory domain (AID) which is present in Group I PAKs. Previous studies in fibroblasts have demonstrated that expression of activated form of PAK-4 promotes cell proliferation, anchorage-independent growth and cell migration, which are the characteristics of malignant tumors. Besides, PAK-4 was found to be frequently overexpressed in tumor cell lines. However, it is still not clear whether PAK-4 plays a role in the pathogenesis of human cancer. Here we report that PAK-4 is frequently over-expressed in hepatocellular carcinomas (HCCs), using real-time quantitative PCR and Western Blotting. To investigate the function of PAK-4 in the development of HCC, we established PAK-4 knocked-down stable cell lines, using vector-based siRNA approach. We report that knocking down of PAK-4 led to decrease in cell migration by trans-well assay. Morphological changes have also been observed after PAK-4 is knocked down. In summary these results incidated a possible tumorigenic effect of PAK-4 in HCC.Further studies are needed to address this issue and provide the molecular mechanism by which PAK-4 activity is regulated.
Persistent Identifierhttp://hdl.handle.net/10722/104787
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorHu, Xen_HK
dc.contributor.authorLeong, VYLen_HK
dc.contributor.authorNg, IOLen_HK
dc.contributor.authorChing, YPen_HK
dc.date.accessioned2010-09-25T22:07:19Z-
dc.date.available2010-09-25T22:07:19Z-
dc.date.issued2006en_HK
dc.identifier.citationThe 97th Annual Meeting of the American Association for Cancer Research (AACR 2006), Washington, DC., 1-5 April 2006. In Cancer Research, 2006, v. 66 n. 8S, p. 1204, abstract no. 5133-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/104787-
dc.description.abstractp21-activated protein kinases (PAKs) are activated by the small Rho family GTPases, Cdc42 and Rac1, in response to various extracellular signals and act in a variety of cellular processes including cell proliferation, morphology, motility, death and survival. PAK-4 is a newly identified Group II member of the PAK family. Like the Group I PAKs, PAK-4 contains an N-terminal p21 binding domain (PBD) and a C-terminal kinase domain, but lacks the auto-inhibitory domain (AID) which is present in Group I PAKs. Previous studies in fibroblasts have demonstrated that expression of activated form of PAK-4 promotes cell proliferation, anchorage-independent growth and cell migration, which are the characteristics of malignant tumors. Besides, PAK-4 was found to be frequently overexpressed in tumor cell lines. However, it is still not clear whether PAK-4 plays a role in the pathogenesis of human cancer. Here we report that PAK-4 is frequently over-expressed in hepatocellular carcinomas (HCCs), using real-time quantitative PCR and Western Blotting. To investigate the function of PAK-4 in the development of HCC, we established PAK-4 knocked-down stable cell lines, using vector-based siRNA approach. We report that knocking down of PAK-4 led to decrease in cell migration by trans-well assay. Morphological changes have also been observed after PAK-4 is knocked down. In summary these results incidated a possible tumorigenic effect of PAK-4 in HCC.Further studies are needed to address this issue and provide the molecular mechanism by which PAK-4 activity is regulated.-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research.-
dc.relation.ispartofCancer Researchen_HK
dc.titleOverexpression of PAK4 in hepatocellular carcinoma (HCC)en_HK
dc.typeConference_Paperen_HK
dc.identifier.emailLeong, VYL: vleong@hkucc.hku.hken_HK
dc.identifier.emailNg, IOL: iolng@hkucc.hku.hken_HK
dc.identifier.emailChing, YP: ypching@hkucc.hku.hken_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.identifier.authorityChing, YP=rp00469en_HK
dc.identifier.hkuros120649en_HK
dc.identifier.volume66-
dc.identifier.issue8 suppl.-
dc.identifier.spage1204, abstract no. 5133-
dc.identifier.epage1204, abstract no. 5133-

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