No conflicts of interest were declared.
Decitabine represses translocated MYC oncogene in Burkitt lymphoma
Article first published online: 22 FEB 2013
Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
The Journal of Pathology
Volume 229, Issue 5, pages 775–783, April 2013
How to Cite
Guan, H., Xie, L., Klapproth, K., Weitzer, C. D., Wirth, T. and Ushmorov, A. (2013), Decitabine represses translocated MYC oncogene in Burkitt lymphoma. J. Pathol., 229: 775–783. doi: 10.1002/path.4164
- Issue published online: 13 MAR 2013
- Article first published online: 22 FEB 2013
- Accepted manuscript online: 23 JAN 2013 05:38AM EST
- Manuscript Accepted: 24 DEC 2012
- Manuscript Revised: 20 DEC 2012
- Manuscript Received: 9 JUL 2012
- Burkitt lymphoma;
Burkitt lymphoma (BL) is caused by translocation of the MYC gene to an immunoglobulin locus resulting in its constitutive expression depending on the activity of the immunoglobulin (Ig) enhancer elements. Treatment of BL cell lines with epigenetic modifiers is known to repress B-cell-specific genes and to up-regulate B-cell-inappropriate genes including the transcription repressor ID2 expression. We found that the DNA methyltransferase inhibitor decitabine/5-aza-2-deoxycytidine (5-aza-dC) represses the MYC oncogene on RNA and protein levels by inducing ID2. Down-regulation of MYC was associated with repression of transcriptional activity of the Ig locus and with inhibition of proliferation. The induction of ID2 can be in part explained by activation of the transcription factor NF-κB. We conclude that up-regulation of ID2 contributes to anti-tumour activity of 5-aza-dC via repression of Ig locus activity and consequently MYC expression. Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.