Role of thrombin receptor in breast cancer invasiveness.

Role of thrombin receptor in breast cancer invasiveness.
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凝血酶受体在乳腺癌侵袭性中的作用。

DOI:
10.1038/sj.bjc.6690063
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发表时间:
1999-02
影响因子:
8.8
通讯作者:
Pentecost, BT
Pentecost, BT
中科院分区:
医学1区
文献类型:
--
作者:
Henrikson, KP;Salazar, SL;Fenton, JW;Pentecost, BT

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侵袭,上皮癌细胞从基底膜分离并移动通过基底膜的能力,是肿瘤转移的中心过程。侵袭的两个组成部分是细胞外基质的蛋白水解和细胞通过它的运动。这两个过程的一个潜在的启动子是凝血酶,一种来源于普遍存在的血浆蛋白凝血酶原的丝氨酸蛋白酶。凝血酶在体外试验中促进MDA-MB 231乳腺肿瘤细胞(一种高度侵袭性细胞系)的侵袭。侵袭性较低的细胞系MDA-MB 436和MCF-7细胞的侵袭不受凝血酶的促进。加入细胞的凝血酶是细胞运动的刺激物;成纤维细胞条件培养基是趋化因子。凝血酶促进的侵袭被水蛭素抑制。侵袭的刺激是由凝血酶受体活化肽模拟的受体介导的过程。凝血酶在体外对趋化性无影响。在MDA-MB 231细胞表面可检测到凝血酶受体,而在其他两种细胞系上则无。在雌二醇存在或不存在的情况下,通过用pHEO转染将雌激素受体引入MDA-MB 231细胞中对凝血酶受体表达没有影响。本文表明,凝血酶增加侵袭性乳腺癌细胞系MDA-MB 231的凝血酶受体依赖性机制的侵袭。© 1999癌症研究运动
Invasion, the ability of an epithelial cancer cell to detach from and move through a basement membrane, is a central process in tumour metastasis. Two components of invasion are proteolysis of extracellular matrix and cellular movement through it. A potential promoter of these two processes is thrombin, the serine proteinase derived from the ubiquitous plasma protein prothrombin. Thrombin promotes the invasion of MDA-MB231 breast tumour cells (a highly aggressive cell line) in an in vitro assay. Invasion by MDA-MB436 and MCF-7 cells, less aggressive cell lines, is not promoted by thrombin. Thrombin, added to the cells, is a stimulator of cellular movement; fibroblast-conditioned medium is the chemotaxin. Thrombin-promoted invasion is inhibited by hirudin. Stimulation of invasion is a receptor-mediated process that is mimicked by a thrombin receptor-activating peptide. Thrombin has no effect on chemotaxis in vitro. Thrombin receptor is detectable on the surface of MDA-MB231 cells, but not on the other two cell lines. Introduction of oestrogen receptors into MDA-MB231 cells by transfection with pHEO had no effect on thrombin receptor expression, in the presence or absence of oestradiol. This paper demonstrates that thrombin increases invasion by the aggressive breast cancer cell line MDA-MB231 by a thrombin receptor-dependent mechanism. © 1999 Cancer Research Campaign
DOI: 10.1002/ijc.2910540514
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