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Nucleic Acids Research Advance Access published online on September 10, 2009
Nucleic Acids Research, doi:10.1093/nar/gkp723
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© The Author(s) 2009. Published by Oxford University Press.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gene Regulation, Chromatin and Epigenetics

MeCP2/H3meK9 are involved in IL-6 gene silencing in pancreatic adenocarcinoma cell lines

Mario Dandrea1,2, Massimo Donadelli1, Chiara Costanzo1, Aldo Scarpa2 and Marta Palmieri1,*

1Department of Morphological and Biomedical Sciences, Section of Biochemistry and 2Department of Pathology, University of Verona, Verona, Italy

*To whom correspondence should be addressed. Tel: +39 045 8027169; Fax: +39 045 8027170; Email: marta.palmieri{at}univr.it

Received January 24, 2008. Revised August 11, 2009. Accepted August 16, 2009.

The aim of the present study was to analyse the molecular mechanisms involved in the Interleukin-6 (IL-6) silencing in pancreatic adenocarcinoma cell lines. Our results demonstrate that TNF-{alpha}, a major IL-6 inducer, is able to induce IL-6 only in three out of six cell lines examined. 5-aza-2'-deoxycytidine (DAC), but not trichostatin A (TSA), activates the expression of IL-6 in all cell lines, indicating that DNA methylation, but not histone deacetylation, plays an essential role in IL-6 silencing. Indeed, the IL-6 upstream region shows a methylation status that correlates with IL-6 expression and binds MeCP2 and H3meK9 only in the non-expressing cell lines. Our results suggest that critical methylations located from positions –666 to –426 relative to the transcription start site of IL-6 may act as binding sites for MeCP2.


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