Dissemin is shutting down on January 1st, 2025

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Oxford University Press, Nucleic Acids Research, 20(37), p. 6681-6690, 2009

DOI: 10.1093/nar/gkp723

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

Journal article published in 2009 by Mario Dandrea, Palmieri M. Scarpa A., Massimo Donadelli ORCID, Chiara Costanzo, Aldo Scarpa ORCID, Marta Palmieri
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

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.