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Papers In Press, published online ahead of print March 26, 2004
Molecular Cancer Biology, Institute of Cancer Biology, Copenhagen DK-2100
Corresponding Author: mg{at}cancer.dk
Causal implication of S100A4 in inducing metastases was convincingly shown previously. However, the mechanisms that associate S100A4 with tumor progression are not well understood. S100A4 protein, as a typical member of the S100 family, exhibits dual, intra- and extracellular, functions. This work is focused on the extracellular function of S100A4, in particular its involvement in tumor-stroma interplay in VMR tumor cells, which exhibit stroma- dependent metastatic phenotype. We demonstrated the reciprocal influence of tumor and stroma cells where tumor cells stimulate S100A4 secretion from fibroblasts in culture. In turn the extracellular S100A4 modifies the cytoskeleton and focal adhesions and triggers several other events in tumor cells. We found stabilization of the tumor suppressor protein p53 and modulation of its function. In particular, extracellular S100A4 down regulates the pro-apoptotic bax and the angiogenesis inhibitor thrombospondin-1 genes. For the first time we demonstrate here that the S100A4 protein added to the extracellular space strongly stimulates proteolytic activity of VMR cells. This activity, most likely, is associated with MMPs and in particular with MMP-13. Finally, application of the recombinant S100A4 protein confers stroma-independent metastatic phenotype on VMR tumor cells. In conclusion, our results indicate that metastasis-inducing S100A4 protein plays a pivotal role in the tumor-stroma environment. S100A4 released either by tumor or stroma cells triggers pro-metastatic cascades in tumor cells.
J. Biol. Chem, 10.1074/jbc.M400441200
Submitted on January 15, 2004
Revised on March 15, 2004
Accepted on March 26, 2004
Functional significance of metastasis-inducing S100A4(Mts1) in tumor-stroma interplay
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