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Centre for Immunology, St. Vincent’s Hospital and University of New South Wales, Victoria Street, Sydney, NSW 2010, Australia [T. L., A. R. B., J. Z., D. A. B., S. P., S. N. B.], and Oncology Research Centre, Prince of Wales Hospital, and Department of Medicine, The University of New South Wales, Randwick, Sydney, New South Wales 2031, Australia [P. J. R.]
Macrophage inhibitory cytokine 1 (MIC-1), a divergent member of the transforming growth factor-ß superfamily, is linked to the pathogenesis of cancer. To delineate possible roles for MIC-1 in prostate cancer, a number of prostate epithelial cell lines have been studied, including PZ-HPV-7, DU-145, PC-3, and LNCaP cells. Factors regulating the production of MIC-1 protein by these cells and some of the effects of MIC-1 on them were investigated. Although PZ-HPV-7 and DU-145 produced no MIC-1 protein, PC-3 and LNCaP cells secreted MIC-1 protein at high levels. The secretion of MIC-1 in LNCaP cells was modulated by both androgen and estrogen. Although neither MIC-1 nor anti-MIC-1 antibody had any effect on the proliferation of epithelial cells, MIC-1 induced changes in DU-145 cells. These cells became flattened and more spread out, and this was accompanied by reduced intercellular actin filaments and intercellular junctions. The DU-145 cells then detached from their substrate and underwent caspase-dependent apoptosis. To define some of the genes responsible for these changes, cDNA microarrays, followed by confirmatory reverse transcription-PCR, was used to analyze differential gene expression induced by MIC-1. The antiapoptotic gene metallothionein 1E and cell adhesion genes RhoE and catenin 
1were down-regulated by more than 2-fold by MIC-1, suggesting that they were, at least in part, responsible for the observed changes in the behavior of DU-145 cells. These findings suggest that although MIC-1 has no effect on cell proliferation, it reduces cell adhesion and consequently induces cell detachment. It is likely that caspase-dependent apoptosis is secondary to loss of cell adhesion and may suggest a role for MIC-1 in tumor dissemination in vivo.
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