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

被引：284

作者：

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 ^{[1
]}

机构：

[1] Nagoya City Univ, Sch Med, Dept Expt Pathol & Tumor Biol, Nagoya, Aichi 4678601, Japan

[2] Vanderbilt Univ, Dept Canc Biol, Nashville, TN 37232 USA

[3] Vanderbilt Univ, VUIIS, Nashville, TN 37232 USA

[4] Nagoya City Univ, Sch Med, Dept Nephrourol, Nagoya, Aichi 4678601, Japan

[5] Univ Nebraska, Med Ctr, Dept Pathol & Microbiol, Omaha, NE 68198 USA

来源：

CANCER CELL | 2005年 / 7卷 / 05期

关键词：

D O I：

10.1016/j.ccr.2005.04.013

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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-cleficient 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.

引用

页码：485 / 496

页数：12

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