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Cancers 2014, 6(3), 1298-1327; doi:10.3390/cancers6031298

Roles of Matrix Metalloproteinases and Their Natural Inhibitors in Prostate Cancer Progression

Division of Hematology and Medical Oncology, The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
Author to whom correspondence should be addressed.
Received: 4 April 2014 / Revised: 31 May 2014 / Accepted: 9 June 2014 / Published: 27 June 2014
(This article belongs to the Special Issue Matrix Metalloproteinases in Cancer Progress)
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Matrix metalloproteinases (MMPs), a group of zinc-dependent endopeptidases involved in the degradation of the extracellular matrix, play an important role in tissue remodeling associated with various physiological processes such as morphogenesis, angiogenesis, and tissue repair, as well as pathological processes including cirrhosis, arthritis and cancer. The MMPs are well established as mediators of tumor invasion and metastasis by breaking down connective tissue barriers. Although there has been a vast amount of literature on the role of MMPs in invasion, metastasis and angiogenesis of various cancers, the role of these endopeptidases in prostate cancer progression has not been systematically reviewed. This overview summarizes findings on the tissue and blood expression of MMPs, their function, regulation and prognostic implication in human prostate cancer, with a focus on MMP-2, -7, -9, MT1-MMP and tissue inhibitor of metalloproteinase 1 (TIMP-1). This review also summarizes the efficacy and failure of early-generation matrix metalloproteinase inhibitors (MMPIs) in the treatment of metastatic prostate cancer and highlights the lessons and challenges for next generation MMPIs.
Keywords: MMP; TIMP; prostate cancer MMP; TIMP; prostate cancer
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Gong, Y.; Chippada-Venkata, U.D.; Oh, W.K. Roles of Matrix Metalloproteinases and Their Natural Inhibitors in Prostate Cancer Progression. Cancers 2014, 6, 1298-1327.

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