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胶质瘤侵袭的机制:基质金属蛋白酶的作用

Mechanisms of glioma invasion: role of matrix-metalloproteinases.

作者信息

Uhm J H, Dooley N P, Villemure J G, Yong V W

机构信息

Department of Neurology & Neurosurgery, Montreal Neurological Institute, McGill University, Canada.

出版信息

Can J Neurol Sci. 1997 Feb;24(1):3-15. doi: 10.1017/s0317167100021028.

DOI:10.1017/s0317167100021028
PMID:9043741
Abstract

One of the most lethal properties of high grade gliomas is their ability to invade the surrounding normal brain tissue, as infiltrated cells often escape surgical resection and inevitably lead to tumour recurrence. The consequent poor prognosis and survival rate underscore the need to further understand and target the cellular mechanisms that underly tumour invasiveness. Proteases which degrade the surrounding stromal cells and extracellular matrix proteins have been demonstrated to be critical effectors of invasion for tumours of both central and peripheral origin. Within the nervous system, the role of metalloproteinases as well as other classes of proteases in mediating the invasive phenotype of high grade gliomas has been an intense area of research. We present in this article a review of this literature and address the possibility that these proteases and the biochemical pathways that regulate their expression, such as protein kinase C, may represent potential targets in the therapy of high grade gliomas.

摘要

高级别胶质瘤最致命的特性之一是其侵袭周围正常脑组织的能力,因为浸润细胞常常逃避手术切除,不可避免地导致肿瘤复发。随之而来的不良预后和生存率凸显了进一步了解并针对肿瘤侵袭性背后的细胞机制的必要性。已证明,降解周围基质细胞和细胞外基质蛋白的蛋白酶是中枢和外周起源肿瘤侵袭的关键效应因子。在神经系统中,金属蛋白酶以及其他类型的蛋白酶在介导高级别胶质瘤侵袭表型方面的作用一直是研究的热点领域。我们在本文中对该文献进行综述,并探讨这些蛋白酶以及调节其表达的生化途径(如蛋白激酶C)可能成为高级别胶质瘤治疗潜在靶点的可能性。

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