Epithelial-mesenchymal transition in prostate cancer and the potential role of kallikrein serine proteases
Epithelial-mesenchymal transition in prostate cancer and the potential role of kallikrein serine proteases
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DOI：
10.1159/000101311
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发表时间：
2007-01-01
影响因子：
2.7
通讯作者：
Clements, Judith A.
中科院分区：
文献类型：
--
作者：
Lawrence, Mitchell G.;Veveris-Lowe, Tara L.;Clements, Judith A.
一旦肿瘤扩散到腺体外，前列腺癌的死亡率就很高。上皮-间质转化（EMT）已被提出促进肿瘤细胞的传播。在这篇文章中，我们总结了EMT在前列腺癌中的证据，利用EMT相关标志物的表达和已知的在其他系统中诱导EMT的因素的功能。我们还讨论了我们最近的研究结果，即组织钾化钾素家族的两个成员，前列腺特异性抗原（PSA/KLK3）和钾化钾素相关肽酶4 (KLK4)，导致PC3前列腺癌细胞的emt样变化。版权所有(c) 2007 S. Karger AG，巴塞尔。
Prostate cancer is associated with significant mortality once the tumour has spread outside the gland. Epithelial-mesenchymal transition (EMT) has been proposed to facilitate this dissemination of tumour cells. In this article we summarize the evidence for EMT in prostate cancer, drawing on the expression of EMT-related markers and the functions of factors known to induce EMT in other systems. We also discuss our recent findings that two members of the tissue kallikrein family of serine proteases, prostate-specific antigen (PSA/KLK3) and kallikrein-related peptidase 4 (KLK4), lead to EMT-like changes in PC3 prostate cancer cells. Copyright (c) 2007 S. Karger AG, Basel.