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Ras癌基因介导的92 kDa金属蛋白酶的诱导;与恶性表型密切相关。

Ras oncogene mediated induction of a 92 kDa metalloproteinase; strong correlation with the malignant phenotype.

作者信息

Ballin M, Gomez D E, Sinha C C, Thorgeirsson U P

机构信息

Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892.

出版信息

Biochem Biophys Res Commun. 1988 Aug 15;154(3):832-8. doi: 10.1016/0006-291x(88)90215-x.

Abstract

We have previously demonstrated that activated ras oncogenes can induce the metastatic phenotype and type IV collagenolytic activity in NIH/3T3 cells (Thorgeirsson et al. Mol. Cell. Biol. 5:259-262, 1985). The present study demonstrates ras-mediated induction of a 92 kDa metalloproteinase, which degrades gelatin and type IV collagen. Association of the 92 kDa proteinase expression with the malignant phenotype was also observed in human tumor cell lines. Our data indicate that the 92 kDa gelatin-collagen IV degrading metalloproteinase is an important participant in the proteolytic process involving tumor cell invasion and metastasis.

摘要

我们先前已证明,激活的ras癌基因可在NIH/3T3细胞中诱导转移表型和IV型胶原酶活性(索尔吉尔松等人,《分子与细胞生物学》5:259 - 262,1985年)。本研究表明,ras介导诱导一种92 kDa的金属蛋白酶,该酶可降解明胶和IV型胶原。在人肿瘤细胞系中也观察到92 kDa蛋白酶的表达与恶性表型相关。我们的数据表明,92 kDa的明胶 - IV型胶原降解金属蛋白酶是涉及肿瘤细胞侵袭和转移的蛋白水解过程中的重要参与者。

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