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

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.

• Authors: Yan Shao, Chang Chun Ling, Xu Qing Liu
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 450 Issue 1 Pg. 227-33 (Jul 18 2014) ISSN: 1090-2104 [Electronic] United States
• PMID: 24878528 (Publication Type: Journal Article)
• Copyright: Copyright © 2014 Elsevier Inc. All rights reserved.

Chemical References

• Antineoplastic Agents, Phytogenic
• BCL6 protein, human
• Carrier Proteins
• DNA-Binding Proteins
• Proto-Oncogene Proteins c-bcl-6
• TXNIP protein, human
• Etoposide
• Caspases
• Glucose

Topics

• 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)
• Proto-Oncogene Proteins c-bcl-6