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Cancer Cell. 2005 May;7(5):485-96.

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

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1
Department of Cancer Biology, Vanderbilt University, Nashville, Tennessee 37232, USA.

Abstract

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.

PMID:
15894268
DOI:
10.1016/j.ccr.2005.04.013
[Indexed for MEDLINE]
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