期刊
NUCLEIC ACIDS RESEARCH
卷 37, 期 20, 页码 6681-6690出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkp723
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资金
- Fondazione Giorgio Zanotto, Verona, Italy
- Associazione Italiana Ricerca sul Cancro, Milan, Italy
- Italian Ministry of University and Research
- University of Verona.
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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