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

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.
AuthorsYan Shao, Chang Chun Ling, Xu Qing Liu
JournalBiochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 450 Issue 1 Pg. 227-33 (Jul 18 2014) ISSN: 1090-2104 [Electronic] United States
PMID24878528 (Publication Type: Journal Article)
CopyrightCopyright © 2014 Elsevier Inc. All rights reserved.
Chemical References
  • Antineoplastic Agents, Phytogenic
  • BCL6 protein, human
  • Carrier Proteins
  • DNA-Binding Proteins
  • TXNIP protein, human
  • Etoposide
  • Caspases
  • Glucose
  • Antineoplastic Agents, Phytogenic (administration & dosage)
  • Apoptosis (drug effects)
  • Carrier Proteins (metabolism)
  • Caspases (metabolism)
  • Cell Line, Tumor
  • DNA-Binding Proteins (metabolism)
  • Dose-Response Relationship, Drug
  • Drug Interactions
  • Etoposide (administration & dosage)
  • Glucose (administration & dosage, pharmacokinetics)
  • Humans
  • Lymphoma, B-Cell (metabolism, pathology)

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