MeCP2/H3meK9 are involved in IL-6 gene silencing in pancreatic adenocarcinoma cell lines.
Nucleic Acids Res
; 37(20): 6681-90, 2009 Nov.
Article
en En
| MEDLINE
| ID: mdl-19745053
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.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Neoplasias Pancreáticas
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Azacitidina
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Adenocarcinoma
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Interleucina-6
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Silenciador del Gen
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Proteína 2 de Unión a Metil-CpG
Límite:
Humans
Idioma:
En
Revista:
Nucleic Acids Res
Año:
2009
Tipo del documento:
Article
País de afiliación:
Italia