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首页> 外文期刊>Cell communication & adhesion >Functional Effect of Contortrostatin, a Snake Venom Disintegrin, on Human Glioma Cell Invasion In Vitro
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Functional Effect of Contortrostatin, a Snake Venom Disintegrin, on Human Glioma Cell Invasion In Vitro

机译：蛇毒Disintegrin Contortrostatin对人胶质瘤细胞体外侵袭的功能作用

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摘要

The metastatic spread of cancer is a complex process that involves the combination of different cellular actions including cell adhesion to the extracellular matrix (ECM), breakdown of the ECM by specific matrix-degrading proteinases, and active ell locomotion. Contortrostatin (CN), a homodimeric snake venom disintegrin, has previously been demonstrated to be effective in blocking vitronectin/fibronectin-dependent adhesion and invasion of T98G human glioblastoma cells through Matrigel using in vitro studies. However, it is not known at what step of the invasion process CN exerts its inhibitory effect. In the present report, CN is shown to decrease invasion of various glioma cell lines through Matrigel affecting neither cell adhesion, nor cell viability. While CN had no effect on cell binding to laminin and type IV collagen, it blocked adhesion of αvβ3-positive, but not αvβ3-negative cells, to vitronectin and fibronectin. Furthermore, members of the matrix metalloproteinase (MMP) family and their physiological inhibitors, and of the plasminogen activator (PA)/plasmin system were demonstrated not to be involved in CN-induced loss of glioma cell invasiveness. Instead, CN inhibited active locomotion of cells on Matrigel. These data suggest that CN-mediated inhibition of glioma cell invasion through Matrigel is a direct result of impaired cell motility. Moreover, use of several glioma cell lines and integrin antibodies strongly indicate the versatility of CN in inhibiting the invasion process based on the ability of CN to interact with different integrins, including αvβ3, αvβ5, and α5β1.
机译：癌症的转移扩散是一个复杂的过程，涉及多种细胞活动的结合，包括细胞对细胞外基质（ECM）的粘附，特定基质降解蛋白酶对ECM的分解以及主动的运动。 Contortrostatin（CN）是一种同二聚体蛇毒双整合素，先前已通过体外研究证明其可通过Matrigel有效地阻断玻连蛋白/纤连蛋白依赖性T98G人胶质母细胞瘤细胞的粘附和侵袭。然而，尚不知道CN在什么过程中发挥其抑制作用。在本报告中，CN显示通过Matrigel减少各种神经胶质瘤细胞系的侵袭，既不影响细胞粘附，也不影响细胞生存力。 CN对细胞与层粘连蛋白和IV型胶原的结合没有影响，但它阻止了αvβ3阳性细胞对玻连蛋白和纤连蛋白的粘附，但对αvβ3阴性细胞没有粘附作用。此外，已证明基质金属蛋白酶（MMP）家族成员及其生理抑制剂以及纤溶酶原激活剂（PA）/纤溶酶系统成员均不参与CN诱导的神经胶质瘤细胞侵袭性丧失。相反，CN抑制了基质胶上细胞的主动运动。这些数据表明CN介导的通过Matrigel抑制神经胶质瘤细胞入侵是细胞运动受损的直接结果。此外，基于CN与包括αvβ3，αvβ5和α5β1在内的不同整联蛋白相互作用的能力，使用多种神经胶质瘤细胞系和整联蛋白抗体强烈表明了CN在抑制侵袭过程中的多功能性。

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