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Matrix metalloproteinase-8 (MMP-8; neutrophil collagenase) is an important regulator of innate immunity that has oncosuppressive actions in numerous tumor types.    Methods  We have intercrossed  Mmp8 -null mice with the Polyoma virus middle T oncogene-driven (MMTV-PyMT) mouse model of mammary cancer to explore the effects of loss of MMP-8 on the incidence and progression of mammary carcinomas.    Results  In this aggressive mouse model of breast cancer, loss of MMP-8 accelerated tumor onset even further, such that 90% of  MMTV-PyMT ;  Mmp8 -null female mice were tumor-bearing at the time of weaning. Throughout the 14 weeks of the model, tumor burden increased in homozygous  Mmp8 -null mice compared to  Mmp8 -wild-type and -heterozygote animals. Likewise, lung metastasis dramatically increased in the  MMTV-PyMT ;  Mmp8 -null mice. Immunohistochemistry revealed that tumors in wild-type,  Mmp8 -heterozygotes and -null animals had similar vascular density at 8 weeks, but at 10 weeks  Mmp8 -wild-type tumors had a lower vascularity than their heterozygote and null counterparts. No differences in macrophage infiltration were apparent throughout primary tumor development, though at 10 weeks a drop in neutrophil infiltrates was observed in  Mmp8 -wild-type tumors. Using quantitative real-time RT-PCR, we tracked the expression of the entire  Mmp  and  Timp  gene families, observing a significant decrease in  Mmp3  expression in  Mmp8 -null tumors compared to wild-type and heterozygotes throughout the time course of the model, which was confirmed at the protein level.    Conclusions  These findings provide novel insight into the suppressive action of MMP-8 on mammary tumorigenesis and metastasis, and indicate that the loss of MMP-8 likely has pleiotropic effects on innate immunity and angiogenesis that are reflected in changes in the protease web.

Pleiotropic functions of the tumor- and metastasis-suppressing matrix metalloproteinase-8 in mammary cancer in MMTV-PyMT transgenic mice