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Department of Veterinary Biosciences [J. A. H., J. W. D.] and Division of Molecular Biology and Cancer Genetics, Ohio State Comprehensive Cancer Center [J. W. D.], The Ohio State University, Columbus, Ohio 43210

Oncostatin M (OSM), an interleukin 6-type cytokine, induces sustained up-regulation of CCAAT/enhancer-binding protein (C/EBP) mRNA and protein in nonneoplastic HC11 mouse mammary epithelial cells. This up-regulation is dependent on signaling by phospho-Stat3 (signal transducers and activators of transcription). The same signaling pathway is activated in two human breast cancer cell lines, a neoplastic mouse mammary epithelial cell line and a second nonneoplastic mouse mammary epithelial cell line. [³H]Thymidine incorporation and flow cytometry demonstrate that OSM inhibits the growth of HC11 cells by reducing the number of S-phase cells. These phenotypic changes are accompanied by reduced expression of S-phase genes with a corresponding increased expression of G₀ genes in HC11 cells. Reduction of C/EBP protein in HC11 cells by expression of a C/EBP antisense construct inhibits OSM-mediated growth arrest. These data demonstrate that OSM induces up-regulation of C/EBP via a Stat3- dependent pathway in mammary epithelial cells and that the growth inhibition induced by OSM depends on the presence of C/EBP.

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