File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL
Supplementary

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 AACR Annual Meeting, Washington, D.C., 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 AACR Annual Meeting, Washington, D.C., 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

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats