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首页> 外文期刊>Seminars in cancer biology >Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs): Positive and negative regulators in tumor cell adhesion.
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Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs): Positive and negative regulators in tumor cell adhesion.

机译：基质金属蛋白酶（MMP）和组织金属蛋白酶抑制剂（TIMP）：肿瘤细胞粘附中的正负调节剂。

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摘要

Cells adhere to one another and/or to matrices that surround them. Regulation of cell-cell (intercellular) and cell-matrix adhesion is tightly controlled in normal cells, however, defects in cell adhesion are common in the majority of human cancers. Multilateral communication among tumor cells with the extracellular matrix (ECM) and neighbor cells is accomplished through adhesion molecules, ECM components, proteolytic enzymes and their endogenous inhibitors. There is sufficient evidence to suggest that reduced adherence is a tumor cell property engaged during tumor progression. Tumor cells acquire the ability to change shape, detach and easily move through spaces disorganizing the normal tissue architecture. This property is due to changes in expression levels of adhesion molecules and/or due to elevated levels of secreted proteolytic enzymes, including matrix metalloproteinases (MMPs). Among other roles, MMPs degrade the ECM and, therefore, prepare the path for tumor cells to migrate, invade and spread to distant secondary areas, where they form metastasis. Tissue inhibitors of metalloproteinases or TIMPs control MMP activities and, therefore, minimize matrix degradation. Both MMPs and TIMPs are involved in tissue remodeling and decisively regulate tumor cell progression including tumor angiogenesis. In this review, we describe and discuss data that support the important role of MMPs and TIMPs in cancer cell adhesion and tumor progression.
机译：细胞彼此粘附和/或粘附在它们周围的基质上。在正常细胞中，细胞间（细胞间）和细胞基质粘附的调节受到严格控制，但是，细胞粘附的缺陷在大多数人类癌症中很常见。肿瘤细胞与细胞外基质（ECM）和邻近细胞之间的多边通讯是通过粘附分子，ECM成分，蛋白水解酶及其内源性抑制剂来实现的。有足够的证据表明减少的依从性是在肿瘤进展期间参与的肿瘤细胞特性。肿瘤细胞具有改变形状，分离并易于在破坏正常组织结构的空间中移动的能力。该性质是由于粘附分子表达水平的变化和/或由于分泌的蛋白水解酶（包括基质金属蛋白酶（MMP））水平升高所致。在其他作用中，MMP使ECM降解，因此为肿瘤细胞迁移，侵袭和扩散到远处的次级区域（在其中形成转移）做好了准备。金属蛋白酶或TIMPs的组织抑制剂可控制MMP活性，因此可将基质降解降至最低。 MMP和TIMP均参与组织重塑，并决定性地调节肿瘤细胞的进程，包括肿瘤血管生成。在这篇综述中，我们描述和讨论了支持MMP和TIMP在癌细胞粘附和肿瘤进展中的重要作用的数据。

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