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Papers In Press, published online ahead of print November 17, 2000
J. Biol. Chem, 10.1074/jbc.M009449200
Submitted on October 17, 2000
Revised on November 17, 2000
Accepted on November 17, 2000
Tumor Biology (H4), Netherlands Cancer Institute, Amsterdam 1066 CX
Corresponding Author: jhi{at}nki.nl
The mucin-like glycoprotein episialin (MUC1) is highly overproduced by a number of human carcinomas. We previously have shown in a variety of mammalian cell lines that overexpression of this very large transmembrane molecule diminishes cellular adhesion, suggesting that episialin/MUC1 overexpression may play an important role in tumor invasion and metastasis. Using in situ hybridization, we show here that episialin/MUC1 mRNA expression can be increased more than 10 fold in breast carcinoma cells relative to the expression in adjacent normal breast epithelium. In search of the molecular mechanism of this overexpression, we observed that the episialin/MUC1 promoter contains a candidate binding site for transcription factors of the STAT-family (STAT = Signal Transducer and Activator of Transcription) approximately 500 bp upstream of the transcription start site. Cytokines and/or growth factors such as interleukin-6 (IL-6) or interferon gamma (IFN-
) can activate STATs. In the human breast carcinoma cell line T47D, both compounds are able to stimulate transcription of a luciferase reporter gene under the control of a 750 bp MUC1 promoter fragment proximal to the transcription start site. The observed increase is entirely mediated by the single STAT-binding site, since mutation of this site abolishes stimulation of the reporter by IL-6 and IFN-. In addition, mutation of the STAT site also decreased the promoter activity in non-stimulated T47D cells, suggesting that the STAT binding site is among the elements that are involved in the overexpression of MUC1 in tumor cells.
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