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首页> 外文期刊>The FEBS journal >CD97 inhibits cell migration in human fibrosarcoma cells by modulating TIMP-2/MT1-MMP/MMP-2 activity - role of GPS autoproteolysis and functional cooperation between the N- and C-terminal fragments
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CD97 inhibits cell migration in human fibrosarcoma cells by modulating TIMP-2/MT1-MMP/MMP-2 activity - role of GPS autoproteolysis and functional cooperation between the N- and C-terminal fragments

机译：CD97通过调节TIMP-2 / MT1-MMP / MMP-2活性来抑制人纤维肉瘤细胞中的细胞迁移-GPS自蛋白水解作用以及N和C末端片段之间的功能协作

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摘要

CD97 is a tumor-associated adhesion-class G-protein-coupled receptor involved in modulating cell migration. Adhesion-class G-protein-coupled receptors are characterized by proteolytic cleavage at a G-protein-coupled receptor proteolysis site (GPS) into an N-terminal fragment (NTF) and a C-terminal fragment (CTF), which remain associated noncovalently. The molecular mechanism and the role of GPS proteolysis in CD97-modulated cell migration are not completely understood. We report here that CD97 expression in HT1080 fibrosarcoma cells enhanced tissue inhibitor of metalloproteinase-2 secretion, leading to reduced membrane type 1 matrix metalloproteinase and matrix metalloproteinase 2 activities. This, in turn, impaired cell migration and invasion in vitro and lung macrometastasis in vivo. CD97 expression also upregulated the expression of integrins, promoting cell adhesion. Importantly, these cellular functions absolutely required the presence of both the NTF and the CTF of CD97, confirming functional cooperation between the two receptor subunits. CD97 gene knockdown reversed these phenotypic changes. We conclude that GPS proteolysis and the functional interplay between the NTF and the CTF are indispensible for CD97 to inhibit HT1080 cell migration by suppressing matrix metalloproteinase activity.
机译：CD97是一种与肿瘤相关的粘附类G蛋白偶联受体，参与调节细胞迁移。粘附类G蛋白偶联受体的特征是在G蛋白偶联受体蛋白水解位点（GPS）上进行蛋白水解切割成N端片段（NTF）和C端片段（CTF），它们保持非共价结合。尚未完全了解CD97调节的细胞迁移中GPS蛋白质水解的分子机制和作用。我们在这里报告，HT1080纤维肉瘤细胞中CD97的表达增强了金属蛋白酶2分泌的组织抑制剂，导致膜1型基质金属蛋白酶和基质金属蛋白酶2活性降低。反过来，这会损害细胞在体外的迁移和侵袭，以及体内肺部大转移。 CD97表达还上调了整联蛋白的表达，从而促进细胞粘附。重要的是，这些细胞功能绝对需要同时存在CD97的NTF和CTF，从而证实了这两个受体亚基之间的功能配合。 CD97基因敲低逆转了这些表型变化。我们得出结论，GPS蛋白水解以及NTF和CTF之间的功能相互作用对于CD97通过抑制基质金属蛋白酶活性抑制HT1080细胞迁移是必不可少的。

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