MMP-7 promotes prostate cancer-induced osteolysis via the solubilization of RANKL. 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, Department of Cancer Biology, Vanderbilt University, Nashville, TN

Jennifer J. Westendorf; Luke Hoeppner

doi:10.1016/j.urolonc.2006.12.003

MMP-7 promotes prostate cancer-induced osteolysis via the solubilization of RANKL. 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, Department of Cancer Biology, Vanderbilt University, Nashville, TN

Jennifer J. Westendorf, Luke Hoeppner

Orthopedic Surgery

Research output: Contribution to journal › Short survey › peer-review

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.

Original language	English (US)
Number of pages	1
Journal	Urologic Oncology: Seminars and Original Investigations
Volume	25
Issue number	2
DOIs	https://doi.org/10.1016/j.urolonc.2006.12.003
State	Published - Mar 1 2007

ASJC Scopus subject areas

Oncology
Urology

Access to Document

10.1016/j.urolonc.2006.12.003

Fingerprint

Dive into the research topics of 'MMP-7 promotes prostate cancer-induced osteolysis via the solubilization of RANKL. 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, Department of Cancer Biology, Vanderbilt University, Nashville, TN'. Together they form a unique fingerprint.

Cite this

Westendorf, J. J., & Hoeppner, L. (2007). MMP-7 promotes prostate cancer-induced osteolysis via the solubilization of RANKL. 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, Department of Cancer Biology, Vanderbilt University, Nashville, TN. Urologic Oncology: Seminars and Original Investigations, 25(2). https://doi.org/10.1016/j.urolonc.2006.12.003

MMP-7 promotes prostate cancer-induced osteolysis via the solubilization of RANKL. 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, Department of Cancer Biology, Vanderbilt University, Nashville, TN. / Westendorf, Jennifer J.; Hoeppner, Luke.
In: Urologic Oncology: Seminars and Original Investigations, Vol. 25, No. 2, 01.03.2007.

Research output: Contribution to journal › Short survey › peer-review

Westendorf, JJ & Hoeppner, L 2007, 'MMP-7 promotes prostate cancer-induced osteolysis via the solubilization of RANKL. 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, Department of Cancer Biology, Vanderbilt University, Nashville, TN', Urologic Oncology: Seminars and Original Investigations, vol. 25, no. 2. https://doi.org/10.1016/j.urolonc.2006.12.003

Westendorf JJ, Hoeppner L. MMP-7 promotes prostate cancer-induced osteolysis via the solubilization of RANKL. 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, Department of Cancer Biology, Vanderbilt University, Nashville, TN. Urologic Oncology: Seminars and Original Investigations. 2007 Mar 1;25(2). doi: 10.1016/j.urolonc.2006.12.003

Westendorf, Jennifer J. ; Hoeppner, Luke. / MMP-7 promotes prostate cancer-induced osteolysis via the solubilization of RANKL. 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, Department of Cancer Biology, Vanderbilt University, Nashville, TN. In: Urologic Oncology: Seminars and Original Investigations. 2007 ; Vol. 25, No. 2.

@article{9b1ce536faa744e3b94c33faf65b08ba,

title = "MMP-7 promotes prostate cancer-induced osteolysis via the solubilization of RANKL. 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, Department of Cancer Biology, Vanderbilt University, Nashville, TN",

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 = "Westendorf, {Jennifer J.} and Luke Hoeppner",

year = "2007",

month = mar,

day = "1",

doi = "10.1016/j.urolonc.2006.12.003",

language = "English (US)",

volume = "25",

journal = "Urologic Oncology",

issn = "1078-1439",

publisher = "Elsevier Inc.",

number = "2",

}

TY - JOUR

T1 - MMP-7 promotes prostate cancer-induced osteolysis via the solubilization of RANKL. 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, Department of Cancer Biology, Vanderbilt University, Nashville, TN

AU - Westendorf, Jennifer J.

AU - Hoeppner, Luke

PY - 2007/3/1

Y1 - 2007/3/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=33847366543&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33847366543&partnerID=8YFLogxK

U2 - 10.1016/j.urolonc.2006.12.003

DO - 10.1016/j.urolonc.2006.12.003

M3 - Short survey

AN - SCOPUS:33847366543

SN - 1078-1439

VL - 25

JO - Urologic Oncology

JF - Urologic Oncology

IS - 2

ER -

Abstract

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this