The skeleton is the most common site of metastasis in patients with advanced prostate cancer. Despite many advances in targeting skeletal metastases, the mechanisms behind the attraction of prostate cancer cells to the bone are not known. Osteoclast cathepsin K, due to its ability to effectively degrade bone matrix collagen I, has been implicated in colonization and growth of prostate tumours in the bone. Identification of new cathepsin K substrates in the bone microenvironment and the recent findings demonstrating its involvement in obesity and inflammation suggest additional roles for this enzyme in skeletal metastases of prostate cancer.
Conference Article| July 20 2007
Cathepsin K in the bone microenvironment: link between obesity and prostate cancer?
I. Podgorski 1
*Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, U.S.A.
†Barbara Ann Karmanos Cancer Institute, Detroit, MI 48201, U.S.A.
1To whom correspondence should be addressed (email firstname.lastname@example.org).
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I. Podgorski, B.E. Linebaugh, B.F. Sloane; Cathepsin K in the bone microenvironment: link between obesity and prostate cancer?. Biochem Soc Trans 1 August 2007; 35 (4): 701–703. doi: https://doi.org/10.1042/BST0350701
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