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

Authors: Lynch, CC  Hikosaka, A  Acuff, HB  Martin, MD  Kawai, N  Singh, RK  Vargo-Gogola, TC  Begtrup, JL  Peterson, TE  Fingleton, B  Shirai, T  Matrisian, LM  Futakuchi, M 
Citation: Lynch CC, etal., Cancer Cell. 2005 May;7(5):485-96.
Pubmed: (View Article at PubMed) PMID:15894268
DOI: Full-text: DOI:10.1016/j.ccr.2005.04.013

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.


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RGD Object Information
RGD ID: 9685352
Created: 2015-01-05
Species: All species
Last Modified: 2015-01-05
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.