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骨微环境中的组织蛋白酶K:肥胖与前列腺癌之间的联系?

Cathepsin K in the bone microenvironment: link between obesity and prostate cancer?

作者信息

Podgorski I, Linebaugh B E, Sloane B F

机构信息

Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA.

出版信息

Biochem Soc Trans. 2007 Aug;35(Pt 4):701-3. doi: 10.1042/BST0350701.

Abstract

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.

摘要

骨骼是晚期前列腺癌患者最常见的转移部位。尽管在靶向骨转移方面取得了许多进展,但前列腺癌细胞向骨骼转移的背后机制尚不清楚。破骨细胞组织蛋白酶K因其有效降解骨基质I型胶原的能力,被认为与前列腺肿瘤在骨中的定植和生长有关。在骨微环境中鉴定新的组织蛋白酶K底物以及最近表明其与肥胖和炎症有关的研究结果,提示了该酶在前列腺癌骨转移中的其他作用。

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