Chelberg M K, McCarthy J B, Skubitz A P, Furcht L T, Tsilibary E C
Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis 55455.
J Cell Biol. 1990 Jul;111(1):261-70. doi: 10.1083/jcb.111.1.261.
The adhesion and motility of tumor cells on basement membranes is a central consideration in tumor cell invasion and metastasis. Basement membrane type IV collagen directly promotes the adhesion and migration of various tumor cell types in vitro. Our previous studies demonstrated that tumor cells adhered and spread on surfaces coated with intact type IV collagen or either of the two major enzymatically purified domains of this protein. Only one of these major domains, the pepsin-generated major triple helical fragment, also supported tumor cell motility in vitro, implicating the involvement of the major triple helical region in type IV collagen-mediated tumor cell invasion in vivo. The present studies extend our previous observations using a synthetic peptide approach. A peptide, designated IV-H1, was derived from a continuous collagenous region of the major triple helical domain of the human alpha 1(IV) chain. This peptide, which has the sequence GVKGDKGNPGWPGAP, directly supported the adhesion, spreading, and motility of the highly metastatic K1735 M4 murine melanoma cell line, as well as the adhesion and spreading of other cell types, in a concentration-dependent manner in vitro. Furthermore, excess soluble peptide IV-H1, or polyclonal antibodies directed against peptide IV-H1, inhibited type IV collagen-mediated melanoma cell adhesion, spreading, and motility, but had no effect on these cellular responses to type I collagen. The full complement of cell adhesion, spreading, and motility promoting activities was dependent upon the preservation of the three prolyl residues in the peptide IV-H1 sequence. These studies indicate that peptide IV-H1 represents a cell-specific adhesion, spreading, and motility promoting domain that is active within the type IV collagen molecule.
肿瘤细胞在基底膜上的黏附与运动能力是肿瘤细胞侵袭和转移的核心考量因素。基底膜IV型胶原在体外能直接促进多种肿瘤细胞类型的黏附与迁移。我们之前的研究表明,肿瘤细胞能黏附并铺展在涂有完整IV型胶原或该蛋白两个主要酶解纯化结构域中任意一个的表面。这些主要结构域中只有一个,即胃蛋白酶产生的主要三螺旋片段,在体外也支持肿瘤细胞的运动能力,这表明主要三螺旋区域参与了IV型胶原介导的体内肿瘤细胞侵袭过程。本研究采用合成肽方法扩展了我们之前的观察结果。一种名为IV - H1的肽,源自人α1(IV)链主要三螺旋结构域的连续胶原区域。该肽序列为GVKGDKGNPGWPGAP,在体外以浓度依赖的方式直接支持高转移性K1735 M4小鼠黑色素瘤细胞系的黏附、铺展和运动能力,以及其他细胞类型的黏附和铺展。此外,过量的可溶性肽IV - H1或针对肽IV - H1的多克隆抗体可抑制IV型胶原介导的黑色素瘤细胞黏附、铺展和运动能力,但对这些细胞对I型胶原的反应没有影响。细胞黏附、铺展和运动促进活性的全部补充依赖于肽IV - H1序列中三个脯氨酰残基的保留。这些研究表明,肽IV - H1代表了一个在IV型胶原分子内具有活性的细胞特异性黏附、铺展和运动促进结构域。