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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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MMP-7 promotes prostate cancer- induced osteolysis via the solubilization of RANKL.

We developed a rodent model that mimics the osteoblastic and osteolytic changes associated with human metastatic prostate cancer. Microarray analysis identified MMP-7, cathepsin-K, and apolipoprotein D as being upregulated at the tumor-bone interface. MMP-7, which was produced by osteoclasts at the tumor-bone interface, was capable of processing RANKL to a soluble form that promoted osteoclast activation. MMP-7-deficient mice demonstrated reduced prostate tumor- induced osteolysis and RANKL processing. This study suggests that inhibition of MMP-7 will have therapeutic benefit in the treatment of prostate cancer-induced osteolysis.[1]

References

  1. MMP-7 promotes prostate cancer-induced osteolysis via the solubilization of RANKL. Lynch, C.C., Hikosaka, A., Acuff, H.B., Martin, M.D., Kawai, N., Singh, R.K., Vargo-Gogola, T.C., Begtrup, J.L., Peterson, T.E., Fingleton, B., Shirai, T., Matrisian, L.M., Futakuchi, M. Cancer Cell (2005) [Pubmed]
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