Interleukin-6 and Leukemia Inhibitory Factor Induction of JunB Is Regulated by Distinct Cell Type-specific Cis-acting Elements

Interleukin (IL)-6 plays an important role in a wide range of biological activities, including differentiation of murine M1 myeloid leukemic cells into mature macrophages. At the onset of M1 differentiation, a set of myeloid differentiation primary response (MyD) genes are induced, including the pro...

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Bibliographic Details
Published in:The Journal of biological chemistry 1999-10, Vol.274 (40), p.28697-28707
Main Authors: Sjin, Robert M. Tjin Tham, Lord, Kenneth A., Abdollahi, Abbas, Hoffman, Barbara, Liebermann, Dan A.
Format: Article
Language:English
Subjects:
Animals
Base Sequence
Binding Sites
DNA
DNA-Binding Proteins - metabolism
Gene Expression Regulation - drug effects
Gene Expression Regulation - genetics
Growth Inhibitors - pharmacology
Interleukin-6 - pharmacology
JunB protein
Leukemia Inhibitory Factor
Lymphokines - pharmacology
Mice
Molecular Sequence Data
myD gene
Promoter Regions, Genetic
Proto-Oncogene Proteins c-jun - genetics
STAT3 Transcription Factor
Trans-Activators - metabolism
Tumor Cells, Cultured
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Summary:Interleukin (IL)-6 plays an important role in a wide range of biological activities, including differentiation of murine M1 myeloid leukemic cells into mature macrophages. At the onset of M1 differentiation, a set of myeloid differentiation primary response (MyD) genes are induced, including the proto-oncogene for JunB. In order to examine the molecular nature of the mechanisms by which IL-6 activates the immediate early expression of MyD genes, JunB was used as a paradigm. A novel IL-6 response element, −65/−52 IL-6RE, to which a 100-kDa protein complex is bound, has been identified on the JunB promoter. Leukemia inhibitory factor (LIF)-induced activation of JunB in M1 cells was also mediated via the −65/−52 IL-6RE. The STAT3 and CRE-like binding sites of the JunB promoter, identified as IL-6-responsive elements in HepG2 liver cells were found, however, to play no role in JunB inducibility by IL-6 in M1 myeloid cells. Conversely, the −65/−52 IL-6RE is shown not to be necessary for JunB inducibility by IL-6 or LIF in liver cells. It appears, therefore, that immediate early activation of JunB is regulated differently in M1 myeloid cells than in HepG2 liver cells. This indicates that distinct cis-acting control elements participate in cell type-specific induction of JunB by members of the IL-6 cytokine superfamily.
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.274.40.28697