Literature DB >> 15894268

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

Conor C Lynch1, Atsuya Hikosaka, Heath B Acuff, Michelle D Martin, Noriyasu Kawai, Rakesh K Singh, Tracy C Vargo-Gogola, Jennifer L Begtrup, Todd E Peterson, Barbara Fingleton, Tomoyuki Shirai, Lynn M Matrisian, Mitsuru Futakuchi.   

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.

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Year:  2005        PMID: 15894268     DOI: 10.1016/j.ccr.2005.04.013

Source DB:  PubMed          Journal:  Cancer Cell        ISSN: 1535-6108            Impact factor:   31.743


  116 in total

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Review 8.  Understanding and targeting osteoclastic activity in prostate cancer bone metastases.

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10.  Study of matrix metalloproteinases and their inhibitors in prostate cancer.

Authors:  S Escaff; J M Fernández; L O González; A Suárez; S González-Reyes; J M González; F J Vizoso
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