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Conference Paper: The biochemical mechanism of hypoxia-induced mobilization of glycogen in cultured cancer cell

TitleThe biochemical mechanism of hypoxia-induced mobilization of glycogen in cultured cancer cell
Authors
Issue Date2014
PublisherBioMed Central Ltd.. The Journal's web site is located at http://www.cancerandmetabolism.com
Citation
The 2014 Metabolism, Diet and Disease Conference, Washington DC., 28-30 May 2014. In Cancer & Metabolism, 2014, v. 2 suppl. 1, abstract P37 How to Cite?
AbstractBACKGROUND: Metabolic reprogramming is one of the strategies adopted by cancer cells to survive hypoxic conditions. Recent findings suggest that hypoxic cancer cells derive the energy that they need through glycolysis using glucose mobilized from intracellular glycogen reserve. Glycogen phosphorylase (GP) is the major rate-determining enzyme for glycogen mobilization in many normal cells under the condition of starvation or physical exercise. The lysosomal alpha-glucosidase (GAA) has also been implicated in glycogen mobilization since deficiency of this enzyme is known to result in Glycogen Storage Disease Type II (Pompe disease). Although a role for GP in the mobilization of glycogen by cancer cells depleted of oxygen had been demonstrated, whether a similar role for GP (and GAA) could be demonstrated under deprivation of both glucose and oxygen is not yet known. This issue is addressed in this study by examining the intracellular level of glycogen in the absence and presence of pharmacological inhibitors of GP and/or …
DescriptionConference Theme: Cancer and metabolism
Poster Presentation: P37
Persistent Identifierhttp://hdl.handle.net/10722/203820
ISSN
2023 Impact Factor: 6.0
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMung, KLen_US
dc.contributor.authorWong, NSen_US
dc.date.accessioned2014-09-19T16:41:13Z-
dc.date.available2014-09-19T16:41:13Z-
dc.date.issued2014en_US
dc.identifier.citationThe 2014 Metabolism, Diet and Disease Conference, Washington DC., 28-30 May 2014. In Cancer & Metabolism, 2014, v. 2 suppl. 1, abstract P37en_US
dc.identifier.issn2049-3002-
dc.identifier.urihttp://hdl.handle.net/10722/203820-
dc.descriptionConference Theme: Cancer and metabolism-
dc.descriptionPoster Presentation: P37-
dc.description.abstractBACKGROUND: Metabolic reprogramming is one of the strategies adopted by cancer cells to survive hypoxic conditions. Recent findings suggest that hypoxic cancer cells derive the energy that they need through glycolysis using glucose mobilized from intracellular glycogen reserve. Glycogen phosphorylase (GP) is the major rate-determining enzyme for glycogen mobilization in many normal cells under the condition of starvation or physical exercise. The lysosomal alpha-glucosidase (GAA) has also been implicated in glycogen mobilization since deficiency of this enzyme is known to result in Glycogen Storage Disease Type II (Pompe disease). Although a role for GP in the mobilization of glycogen by cancer cells depleted of oxygen had been demonstrated, whether a similar role for GP (and GAA) could be demonstrated under deprivation of both glucose and oxygen is not yet known. This issue is addressed in this study by examining the intracellular level of glycogen in the absence and presence of pharmacological inhibitors of GP and/or …-
dc.languageengen_US
dc.publisherBioMed Central Ltd.. The Journal's web site is located at http://www.cancerandmetabolism.com-
dc.relation.ispartofCancer & Metabolismen_US
dc.rightsCancer & Metabolism. Copyright © BioMed Central Ltd..-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleThe biochemical mechanism of hypoxia-induced mobilization of glycogen in cultured cancer cellen_US
dc.typeConference_Paperen_US
dc.identifier.emailWong, NS: nswong@hku.hken_US
dc.identifier.authorityWong, NS=rp00340en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1186/2049-3002-2-S1-P37en_US
dc.identifier.hkuros238596en_US
dc.identifier.volume2-
dc.identifier.issuesuppl. 1-
dc.identifier.isiWOS:000217121500060-
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl2049-3002-

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