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- Publisher Website: 10.1016/j.bbrc.2014.05.096
- Scopus: eid_2-s2.0-84904736866
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Article: High concentrations of glucose suppress etoposide-induced cell death of B-cell lymphoma through BCL-6
Title | High concentrations of glucose suppress etoposide-induced cell death of B-cell lymphoma through BCL-6 |
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Authors | |
Keywords | B-cell lymphoma BCL-6 Chemotherapy Etoposide Glucose |
Issue Date | 2014 |
Publisher | Academic 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? |
Abstract | Glucose 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 Identifier | http://hdl.handle.net/10722/198109 |
ISSN | 2023 Impact Factor: 2.5 2023 SCImago Journal Rankings: 0.770 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Shao, Y | en_US |
dc.contributor.author | Ling, C | en_US |
dc.contributor.author | Liu, X | en_US |
dc.date.accessioned | 2014-06-25T02:47:31Z | - |
dc.date.available | 2014-06-25T02:47:31Z | - |
dc.date.issued | 2014 | en_US |
dc.identifier.citation | Biochemical and Biophysical Research Communications, 2014 | en_US |
dc.identifier.issn | 0006-291X | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/198109 | - |
dc.description.abstract | Glucose 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.language | eng | en_US |
dc.publisher | Academic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description | en_US |
dc.relation.ispartof | Biochemical and Biophysical Research Communications | en_US |
dc.rights | NOTICE: 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.subject | B-cell lymphoma | - |
dc.subject | BCL-6 | - |
dc.subject | Chemotherapy | - |
dc.subject | Etoposide | - |
dc.subject | Glucose | - |
dc.title | High concentrations of glucose suppress etoposide-induced cell death of B-cell lymphoma through BCL-6 | en_US |
dc.type | Article | en_US |
dc.identifier.email | Shao, Y: yshao@hku.hk | en_US |
dc.identifier.email | Ling, C: lingcc@connect.hku.hk | en_US |
dc.identifier.email | Liu, X: xqliu@hku.hk | en_US |
dc.identifier.doi | 10.1016/j.bbrc.2014.05.096 | en_US |
dc.identifier.scopus | eid_2-s2.0-84904736866 | - |
dc.identifier.hkuros | 229259 | en_US |
dc.identifier.isi | WOS:000343641000038 | - |
dc.publisher.place | United States | en_US |
dc.identifier.issnl | 0006-291X | - |