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Article: High concentrations of glucose suppress etoposide-induced cell death of B-cell lymphoma through BCL-6

TitleHigh concentrations of glucose suppress etoposide-induced cell death of B-cell lymphoma through BCL-6
Authors
Issue Date2014
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description
Citation
Biochemical and Biophysical Research Communications, 2014 How to Cite?
AbstractGlucose is potentially a factor in the resistance to chemotherapy of B-cell lymphomas. In this study we investigated the expression of the glucose induced transcription factor Bcl-6 and the underlying mechanism by which it suppresses B-cell lymphoma cell death. Glucose was found to prevent etoposide-induced tumor cell death. BCL-6 expression was induced by glucose but down-regulated by etoposide. BCL-6 expression was regulated by the interaction of VDUP1 and p53. The molecular mechanism by which glucose prevented etoposide-induced tumor cell death was shown to involve the BCL-6 mediated caspase pathway. Our data suggest that glucose-induced BCL-6 overexpression could abrogate the etoposide chemotherapy effect on tumor cell death.
Persistent Identifierhttp://hdl.handle.net/10722/198109
ISSN
2015 Impact Factor: 2.371
2015 SCImago Journal Rankings: 1.152

 

DC FieldValueLanguage
dc.contributor.authorShao, Yen_US
dc.contributor.authorLing, Cen_US
dc.contributor.authorLiu, Xen_US
dc.date.accessioned2014-06-25T02:47:31Z-
dc.date.available2014-06-25T02:47:31Z-
dc.date.issued2014en_US
dc.identifier.citationBiochemical and Biophysical Research Communications, 2014en_US
dc.identifier.issn0006-291Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/198109-
dc.description.abstractGlucose is potentially a factor in the resistance to chemotherapy of B-cell lymphomas. In this study we investigated the expression of the glucose induced transcription factor Bcl-6 and the underlying mechanism by which it suppresses B-cell lymphoma cell death. Glucose was found to prevent etoposide-induced tumor cell death. BCL-6 expression was induced by glucose but down-regulated by etoposide. BCL-6 expression was regulated by the interaction of VDUP1 and p53. The molecular mechanism by which glucose prevented etoposide-induced tumor cell death was shown to involve the BCL-6 mediated caspase pathway. Our data suggest that glucose-induced BCL-6 overexpression could abrogate the etoposide chemotherapy effect on tumor cell death.en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/descriptionen_US
dc.relation.ispartofBiochemical and Biophysical Research Communicationsen_US
dc.rightsNOTICE: this is the author’s version of a work that was accepted for publication in <Journal title>. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in PUBLICATION, [VOL#, ISSUE#, (DATE)] DOI#en_US
dc.titleHigh concentrations of glucose suppress etoposide-induced cell death of B-cell lymphoma through BCL-6en_US
dc.typeArticleen_US
dc.identifier.emailShao, Y: yshao@hku.hken_US
dc.identifier.emailLing, C: lingcc@connect.hku.hken_US
dc.identifier.emailLiu, X: xqliu@hku.hken_US
dc.identifier.doi10.1016/j.bbrc.2014.05.096en_US
dc.identifier.hkuros229259en_US
dc.publisher.placeUnited Statesen_US

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