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

[1]  L. Matrisian,et al.  Matrix metalloproteinases in tumor-host cell communication. , 2002, Differentiation; research in biological diversity.

[2]  V. Stewart,et al.  RAG-2-deficient mice lack mature lymphocytes owing to inability to initiate V(D)J rearrangement , 1992, Cell.

[3]  S. Yamasaki,et al.  Protein expression and functional difference of membrane-bound and soluble receptor activator of NF-kappaB ligand: modulation of the expression by osteotropic factors and cytokines. , 2000, Biochemical and biophysical research communications.

[4]  A. Mizokami,et al.  Osteoprotegerin inhibits prostate cancer-induced osteoclastogenesis and prevents prostate tumor growth in the bone. , 2001, The Journal of clinical investigation.

[5]  B. Fingleton,et al.  Matrix Metalloproteinase Inhibitors and Cancer—Trials and Tribulations , 2002, Science.

[6]  Gabriele Bergers,et al.  MMP-9/Gelatinase B Is a Key Regulator of Growth Plate Angiogenesis and Apoptosis of Hypertrophic Chondrocytes , 1998, Cell.

[7]  S. Kukreja,et al.  Patterns of metastasis by the human prostate cancer cell line PC‐3 in athymic nude mice , 1989, The Prostate.

[8]  K. Pienta,et al.  Antimetastatic drugs in prostate cancer. , 2002, Clinical prostate cancer.

[9]  E. Keller,et al.  Prostate cancer bone metastases promote both osteolytic and osteoblastic activity , 2004, Journal of cellular biochemistry.

[10]  R. Vessella,et al.  Osteoprotegerin and rank ligand expression in prostate cancer. , 2001, Urology.

[11]  R. Vessella,et al.  Establishment and characterization of osseous prostate cancer models: Intra‐tibial injection of human prostate cancer cells , 2002, The Prostate.

[12]  Tadashi Yamamoto,et al.  Molecular Cloning of a New Aquaporin from Rat Pancreas and Liver* , 1997, The Journal of Biological Chemistry.

[13]  R. Fridman,et al.  Matrix metalloproteinase activity, bone matrix turnover, and tumor cell proliferation in prostate cancer bone metastasis. , 2002, Journal of the National Cancer Institute.

[14]  I. Kola,et al.  Cathepsin K Knockout Mice Develop Osteopetrosis Due to a Deficit in Matrix Degradation but Not Demineralization , 1999, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[15]  L. Matrisian,et al.  Differential expression of matrilysin and cyclooxygenase‐2 in intestinal and colorectal neoplasms , 1999, Molecular carcinogenesis.

[16]  Satoru Takahashi,et al.  Establishment of Transplantable Rat Prostate Carcinomas from Primary Lesions Induced by 3,2'-Dimethyl-4-aminobiphenyl and Testosterone , 1998 .

[17]  Nils Brünner,et al.  Synthetic matrix metalloproteinase inhibitors inhibit growth of established breast cancer osteolytic lesions and prolong survival in mice. , 2002, Clinical cancer research : an official journal of the American Association for Cancer Research.

[18]  A. Tumber,et al.  Stromelysin (MMP‐3) Synthesis Is Up‐Regulated in Estrogen‐Deficient Mouse Osteoblasts In Vivo and In Vitro , 1999, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[19]  L. Chung,et al.  Establishment of human prostate carcinoma skeletal metastasis models , 2000, Cancer.

[20]  C. Blobel,et al.  Catalytic Properties of ADAM19* , 2003, Journal of Biological Chemistry.

[21]  J. Delaissé,et al.  Matrix metalloproteinases (MMP) and cathepsin K contribute differently to osteoclastic activities , 2003, Microscopy research and technique.

[22]  N. Greenberg,et al.  A Transgenic Mouse Prostate Cancer Model , 1996, Toxicologic pathology.

[23]  G Shimamoto,et al.  Osteoprotegerin: A Novel Secreted Protein Involved in the Regulation of Bone Density , 1997, Cell.

[24]  D. Grignon,et al.  Severe combined immunodeficient-hu model of human prostate cancer metastasis to human bone. , 1999, Cancer research.

[25]  H. Yasuda,et al.  Transgenic mice overexpressing soluble osteoclast differentiation factor (sODF) exhibit severe osteoporosis , 2002, Journal of Bone and Mineral Metabolism.

[26]  R. Nagle,et al.  Interleukin-1β Secreted from Monocytic Cells Induces the Expression of Matrilysin in the Prostatic Cell Line LNCaP* , 1997, The Journal of Biological Chemistry.

[27]  K. Imaida,et al.  Prostate carcinomas developing in transgenic rats with SV40 T antigen expression under probasin promoter control are strictly androgen dependent. , 2001, Cancer research.

[28]  L. Lum,et al.  Biochemical and Pharmacological Criteria Define Two Shedding Activities for TRANCE/OPGL That Are Distinct from the Tumor Necrosis Factor α Convertase* , 2001, The Journal of Biological Chemistry.

[29]  Mahboob Rahman,et al.  Critical roles for collagenase-3 (Mmp13) in development of growth plate cartilage and in endochondral ossification. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[30]  G. Mundy Metastasis: Metastasis to bone: causes, consequences and therapeutic opportunities , 2002, Nature Reviews Cancer.

[31]  B. Hogan,et al.  Intestinal tumorigenesis is suppressed in mice lacking the metalloproteinase matrilysin. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[32]  R. Baggs,et al.  A murine model of experimental metastasis to bone and bone marrow. , 1988, Cancer research.

[33]  S. Reddy,et al.  Characterization of Immortalized Osteoclast Precursors Developed from Mice Transgenic for Both bcl-XL and Simian Virus 40 Large T Antigen. , 1999, Endocrinology.

[34]  J. Goldman,et al.  Autologous stem cell transplantation normalizes abnormal bone remodeling and sRANKL/osteoprotegerin ratio in patients with multiple myeloma , 2004, Leukemia.

[35]  G. Risbridger,et al.  An in vivo model of prostate carcinoma growth and invasion in bone , 2002, Cell and Tissue Research.

[36]  P. Watson,et al.  A matrix metalloproteinase inhibitor, batimastat, retards the development of osteolytic bone metastases by MDA-MB-231 human breast cancer cells in Balb C nu/nu mice. , 2001, European journal of cancer.