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Conference Paper: Overexpression of AMPKgamma 2 enhances tumorigenicity of Ovarian Cancer Cells

TitleOverexpression of AMPKgamma 2 enhances tumorigenicity of Ovarian Cancer Cells
Authors
Issue Date2008
PublisherAmerican Association for Cancer Research
Citation
AACR 99th Annual Meeting, San Diego, CA, 12-16 April 2008. In Cancer Research, 2008, v. 68 n. 9S, Abstract no. 2737 How to Cite?
AbstractAMP-activated protein kinase (AMPK) is a highly conserved serine-threonine protein kinase which acts as a sensor monitoring cellular energy status and to maintain energy homeostasis in eukaryotic cells. It is activated under a variety of metabolic stresses such as hypoxia, glucose starvation and heat shock etc. Recent findings have shown that artificially activated AMPK by 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR) can strongly inhibit cell proliferation in tumor cells via cell cycle arrest and/or suppression of biosynthetic processes. However, the response varies in different cancer cell types. In the present study, we characterized the functions of AMPKγ2, one of the AMPK subunits, in human ovarian cancer cells. By quantitative RT-PCR and Western blot analyses, we found that the expression levels of AMPKγ2 were higher in human ovarian cancer samples, but were diminished under hypoxia or glucose deprivation treatments. Transient or stably overexpressed AMPKγ2 remarkably reduced the levels of phospho-AMPK (p-AMPK) and the AMPK downstream target, phospho-acetyl-CoA carboxylase (p-ACC), in human ovarian cancer cells. Intriguingly, enforced expression of AMPKγ2 significantly increased cell proliferation, anchorage-independent growth ability, and resistance to the growth-suppressive effect of AICAR. Altogether, these results suggest that AMPKγ2, acts as a negative regulator of AMPK, retards the responses to AICAR treatments, and enhances tumorigenicity of ovarian cancer.
Persistent Identifierhttp://hdl.handle.net/10722/113494
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorChan, DWen_HK
dc.contributor.authorLee, YWen_HK
dc.contributor.authorLiu, VWSen_HK
dc.contributor.authorNgan, HYSen_HK
dc.date.accessioned2010-09-26T04:18:20Z-
dc.date.available2010-09-26T04:18:20Z-
dc.date.issued2008en_HK
dc.identifier.citationAACR 99th Annual Meeting, San Diego, CA, 12-16 April 2008. In Cancer Research, 2008, v. 68 n. 9S, Abstract no. 2737-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/113494-
dc.description.abstractAMP-activated protein kinase (AMPK) is a highly conserved serine-threonine protein kinase which acts as a sensor monitoring cellular energy status and to maintain energy homeostasis in eukaryotic cells. It is activated under a variety of metabolic stresses such as hypoxia, glucose starvation and heat shock etc. Recent findings have shown that artificially activated AMPK by 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR) can strongly inhibit cell proliferation in tumor cells via cell cycle arrest and/or suppression of biosynthetic processes. However, the response varies in different cancer cell types. In the present study, we characterized the functions of AMPKγ2, one of the AMPK subunits, in human ovarian cancer cells. By quantitative RT-PCR and Western blot analyses, we found that the expression levels of AMPKγ2 were higher in human ovarian cancer samples, but were diminished under hypoxia or glucose deprivation treatments. Transient or stably overexpressed AMPKγ2 remarkably reduced the levels of phospho-AMPK (p-AMPK) and the AMPK downstream target, phospho-acetyl-CoA carboxylase (p-ACC), in human ovarian cancer cells. Intriguingly, enforced expression of AMPKγ2 significantly increased cell proliferation, anchorage-independent growth ability, and resistance to the growth-suppressive effect of AICAR. Altogether, these results suggest that AMPKγ2, acts as a negative regulator of AMPK, retards the responses to AICAR treatments, and enhances tumorigenicity of ovarian cancer.-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Researchen_HK
dc.titleOverexpression of AMPKgamma 2 enhances tumorigenicity of Ovarian Cancer Cellsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailChan, DW: dwchan@hkucc.hku.hken_HK
dc.identifier.emailLiu, VWS: vwsliu@hkusua.hku.hken_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.authorityChan, DW=rp00543en_HK
dc.identifier.authorityLiu, VWS=rp00341en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.identifier.hkuros141145en_HK

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