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.