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|Titolo:||Nuclear factor kappa-B (NF-kappa-B), nuclear factor interleukin-6 (NFIL-6 or C/EBP-beta) and nuclear factor interleukin-6-beta (NFIL6-beta or C/EBP-delta) are not sufficient to activate the endogenous interleukin-6 gene in the human breast carcinoma cell|
|Autori interni:||MEROLA, Marcello|
|Data di pubblicazione:||1996|
|Rivista:||EUROPEAN JOURNAL OF BIOCHEMISTRY|
|Abstract:||A comparative study of the molecular mechanism of interleukin-6 (IL-6) gene induction on two breast-carcinoma-derived cell lines has been performed. MDA-MB-231 cells produce constitutive detectable levels of both secreted IL-6 and mRNA which, as expected, are dramatically enhanced following induction by either IL-1-beta or tumor necrosis factor-alpha (TNF-alpha). The levels of both secreted IL-6 and IL-6 mRNA are significantly higher in response to IL-1-beta in spite of the fact that stimulation by TNF-alpha alone enhances the half life of IL-6 mRNA. The protein synthesis inhibitor cycloheximide is also a fairly strong inducer of IL-6 in these cells. In contrast. MCF-7 cells fail to produce detectable IL-6 protein or mRNA, even after stimulation with proper inducers. Analysis of transcription factors NF-kappa-B, NFIL6 and NFIL6-beta. which have been described to be sufficient to activate the IL-6 gene in other cell systems, shows a similar pattern of expression in both MCF-7 and MDA-MB-231 cells. Furthermore, transfection of a recombinant plasmid carrying the IL-6 promoter linked to a luciferase reporter gene shows that both cell lines are able to drive IL-1-beta or TNF-alpha activation of this construction in a very similar manner. Finally, when MCF-7 cells were treated with IL-1-beta or TNF-alpha in the presence of cycloheximide. transcription of IL-6 mRNA from the endogenous IL-6 gene was observed. These data suggest that a mechanism of IL-6 gene repression is active in MCF-7 cells.|
|Appare nelle tipologie:||01.01 Articolo in Rivista|
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