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尿激酶型纤溶酶原激活剂对于前列腺癌细胞的侵袭是必要的,但并不充分。

Urokinase plasminogen activator is necessary but not sufficient for prostate cancer cell invasion.

作者信息

Jarrard D F, Hansen N M, Patai B, Rukstalis D B

机构信息

Department of Surgery, University of Chicago, Il. 60637, USA.

出版信息

Invasion Metastasis. 1995;15(1-2):34-45.

PMID:7672930
Abstract

The expression and function of urokinase plasminogen activator (uPA), an extracellular protease, were examined in four established prostate cancer lines, and one uPA-transfected cell line. The cell lines exhibited variable efficiency in uPA transcription, translation and specific proteolytic activity. A statistically significant inhibition of Boyden chamber invasion by anti-uPA monoclonal antibodies was demonstrated in cell lines TSU-PR1 and PC3. This inhibition suggests a direct role for uPA in the invasion of prostate cancer. However, variable processing of uPA mRNA, protein and proteolytic activity make prediction of in vitro invasion of prostate cancer difficult. Stable transfection experiments suggest that the proteolytic cascade generated by a cell is multiform and solitary alterations in uPA may not modify the proteolytic capability for invasion.

摘要

研究了细胞外蛋白酶尿激酶型纤溶酶原激活剂(uPA)在四种已建立的前列腺癌细胞系和一种uPA转染细胞系中的表达及功能。这些细胞系在uPA转录、翻译和特异性蛋白水解活性方面表现出不同的效率。在TSU-PR1和PC3细胞系中,抗uPA单克隆抗体对博伊登小室侵袭具有统计学意义的抑制作用。这种抑制表明uPA在前列腺癌侵袭中起直接作用。然而,uPA mRNA、蛋白质和蛋白水解活性的可变加工使得预测前列腺癌的体外侵袭变得困难。稳定转染实验表明,细胞产生的蛋白水解级联是多样的,uPA的单独改变可能不会改变侵袭的蛋白水解能力。

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引用本文的文献

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Downregulation of uPA, uPAR and MMP-9 using small, interfering, hairpin RNA (siRNA) inhibits glioma cell invasion, angiogenesis and tumor growth.使用小干扰发夹RNA(siRNA)下调尿激酶型纤溶酶原激活物(uPA)、尿激酶型纤溶酶原激活物受体(uPAR)和基质金属蛋白酶-9(MMP-9)可抑制胶质瘤细胞的侵袭、血管生成和肿瘤生长。
Neuron Glia Biol. 2004 May;1(2):165-76. doi: 10.1017/s1740925x04000237.
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RNAi-mediated downregulation of urokinase plasminogen activator and its receptor in human meningioma cells inhibits tumor invasion and growth.RNA干扰介导的人脑膜瘤细胞中尿激酶型纤溶酶原激活剂及其受体的下调抑制肿瘤侵袭和生长。
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