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Conference Paper: The tumor suppressive function of AMPK in hepatocellular carcinoma

TitleThe tumor suppressive function of AMPK in hepatocellular carcinoma
Authors
Issue Date2007
PublisherAmerican Association for Cancer Research
Citation
American Association for Cancer Research Annual Meeting, Los Angeles, CA, 14-18 April 2007. In Cancer Research, 2007, v. 67, Abstract no. 3686 How to Cite?
AbstractHepatocellular carcinoma (HCC) is one of the most common cancers in the world. However, the molecular mechanism underlying the development of HCC is still unclear. AMP-activated protein kinase (AMPK), which is a serine/theronine protein kinase, originally found as a key regulator in glucose and lipid metabolism in response to cellular stress. Recent publications suggest that AMPK activation results in suppressing cell proliferation. Also, AMPK lies upstream and downstream of two tumor suppressors, TSC2 and LKB1, respectively, indicating that AMPK may also involve in carcinogenesis. In this project, we aim to study the molecular mechanism leading to the tumor suppressive function of AMPK in HCC, particularly relating to the p53 pathway. Our preliminary findings have shown that overexpression of AMPKα2 catalytic subunit in HCC cell line HepG2 suppress cell proliferation in focus formation assay. On the other hand, an increase in proliferation rate was observed in HCC cell with AMPKα2 stably knocked down by small hairpin RNA. Also, our data have demonstrated that expression of constitutive active form of AMPKα2 leads to p53 phosphorylation at serine 15 residue and acetylation at lysine 382 residue. In addition, in-vitro kinase assay has shown that AMPK directly phosphorylates p53. Our results suggest that AMPK may mediate its tumor suppression function through regulation of p53.
Persistent Identifierhttp://hdl.handle.net/10722/94946
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorLiu, MHFen_HK
dc.contributor.authorLeong, VYLen_HK
dc.contributor.authorNg, IOLen_HK
dc.contributor.authorChing, YPen_HK
dc.date.accessioned2010-09-25T15:46:50Z-
dc.date.available2010-09-25T15:46:50Z-
dc.date.issued2007en_HK
dc.identifier.citationAmerican Association for Cancer Research Annual Meeting, Los Angeles, CA, 14-18 April 2007. In Cancer Research, 2007, v. 67, Abstract no. 3686-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/94946-
dc.description.abstractHepatocellular carcinoma (HCC) is one of the most common cancers in the world. However, the molecular mechanism underlying the development of HCC is still unclear. AMP-activated protein kinase (AMPK), which is a serine/theronine protein kinase, originally found as a key regulator in glucose and lipid metabolism in response to cellular stress. Recent publications suggest that AMPK activation results in suppressing cell proliferation. Also, AMPK lies upstream and downstream of two tumor suppressors, TSC2 and LKB1, respectively, indicating that AMPK may also involve in carcinogenesis. In this project, we aim to study the molecular mechanism leading to the tumor suppressive function of AMPK in HCC, particularly relating to the p53 pathway. Our preliminary findings have shown that overexpression of AMPKα2 catalytic subunit in HCC cell line HepG2 suppress cell proliferation in focus formation assay. On the other hand, an increase in proliferation rate was observed in HCC cell with AMPKα2 stably knocked down by small hairpin RNA. Also, our data have demonstrated that expression of constitutive active form of AMPKα2 leads to p53 phosphorylation at serine 15 residue and acetylation at lysine 382 residue. In addition, in-vitro kinase assay has shown that AMPK directly phosphorylates p53. Our results suggest that AMPK may mediate its tumor suppression function through regulation of p53.-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Researchen_HK
dc.titleThe tumor suppressive function of AMPK in hepatocellular carcinomaen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailLiu, MHF: micoliu@hkusua.hku.hken_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.hkuros131612en_HK

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