Author/Authors :
Lynch، نويسنده , , Conor C. and Hikosaka، نويسنده , , Atsuya and Acuff، نويسنده , , Heath B. and Martin، نويسنده , , Michelle D. and Kawai، نويسنده , , Noriyasu and Singh، نويسنده , , Rakesh K. and Vargo-Gogola، نويسنده , , Tracy C. and Begtrup، نويسنده , , Jennifer L. and Peterson، نويسنده , , Todd E. and Fingleton، نويسنده , , Barbara and Shirai، نويسنده , , Tomoyuki and Matrisian، نويسنده , , Lynn M. and Futakuchi، نويسنده , , Mitsuru، نويسنده ,
Abstract :
Summary
eloped 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.
