@article{89f7fb6ced434aeeb7cf8fa3dd4aff80,
title = "MMP-7 promotes prostate cancer-induced osteolysis via the solubilization of RANKL",
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.",
author = "Lynch, {Conor C.} and Atsuya Hikosaka and Acuff, {Heath B.} and Martin, {Michelle D.} and Noriyasu Kawai and Singh, {Rakesh K.} and Vargo-Gogola, {Tracy C.} and Begtrup, {Jennifer L.} and Peterson, {Todd E.} and Barbara Fingleton and Tomoyuki Shirai and Matrisian, {Lynn M.} and Mitsuru Futakuchi",
note = "Funding Information: This work was supported by a grant from the NIH (R01 84360 to LMM), Grants-in-Aid for Cancer Research from the Ministry of Education, Culture, Sports, Science, and Technology and the Ministry of Health, Labor, and Welfare, Japan, a Grant-in-aid from the Ministry of Health, Labor and Welfare for the Second-Term Comprehensive 10-Year Strategy for Cancer Control, Japan, and a grant from the Society for Promotion of Pathology of Nagoya, Japan. C.C.L. is supported by grant PDF02-1394 awarded by the Susan G. Komen Breast Cancer Foundation. We also thank Oliver McIntyre and Lisa McCawley for their valuable critique.",
year = "2005",
month = may,
doi = "10.1016/j.ccr.2005.04.013",
language = "English (US)",
volume = "7",
pages = "485--496",
journal = "Cancer Cell",
issn = "1535-6108",
publisher = "Cell Press",
number = "5",
}