EPIDERMAL GROWTH-FACTOR ENHANCEMENT OF HSC-1 HUMAN CUTANEOUS SQUAMOUS CARCINOMA CELL-ADHESION AND MIGRATION ON TYPE-I COLLAGEN INVOLVES SELECTIVE UP-REGULATION OF ALPHA(2),BETA(1) INTEGRIN EXPRESSION
EPIDERMAL GROWTH-FACTOR ENHANCEMENT OF HSC-1 HUMAN CUTANEOUS SQUAMOUS CARCINOMA CELL-ADHESION AND MIGRATION ON TYPE-I COLLAGEN INVOLVES SELECTIVE UP-REGULATION OF ALPHA(2),BETA(1) INTEGRIN EXPRESSION
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DOI：
10.1006/excr.1995.1032
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发表时间：
1995-01-01
影响因子：
3.7
通讯作者：
IMAMURA, S
中科院分区：
文献类型：
--
作者：
FUJII, K;DOUSAKANAKAJIMA, N;IMAMURA, S
一些人类肿瘤表现出表皮生长因子（EGF）受体的异常表达或过度表达，并且受体表达的程度与某些上皮肿瘤（包括鳞状癌细胞）的恶性表型相关。由于细胞的表型转化可能涉及整合素功能的定量和定性改变，因此使用 HSC-1 细胞（一种显示 EGF 受体过度表达的人类鳞状癌细胞系）研究了 EGF 对细胞-基质相互作用的影响。细胞粘附和吞噬动力学轨迹测定表明，经 EGF 处理的 HSC-1 细胞与基质蛋白的相互作用与未处理的细胞不同。在纤连蛋白、层粘连蛋白、纤维蛋白原和 I 型胶原中，纤连蛋白是促进未经处理的 HSC-1 细胞粘附和迁移的最有效基质。用 50 ng/ml EGF 预处理细胞 18 小时，选择性地将 I 型胶原上扩散细胞的数量和单个细胞迁移区域的大小分别增加 250% 和 400%。相同的预处理减少了其他基质上的细胞粘附和迁移，因此EGF处理将I型胶原转化为HSC-1细胞的细胞粘附和迁移的最有效基质。 ELISA和免疫沉淀研究表明，EGF通过刺激α(2)亚基的生物合成，以时间和剂量依赖性方式上调α(2)β(1)整合素胶原蛋白受体的表达，但不上调α(3)β(1)、α(5)β(1)或α(v)的表达 β(3)，整合素。这些结果表明，EGF 优先增强 HSC-1 细胞与 I 型胶原的相互作用，导致细胞在基质上的迁移活性增强，这是选择性上调 α(2) beta 1( ) 整合素表达的结果。 (C) 1995 学术出版社
Some human neoplasms show aberrant expression or overexpression of epidermal growth factor (EGF) receptor, and the degree of the receptor expression is correlated with the malignant phenotype in certain epithelial tumors including squamous carcinoma cells. Since phenotypic transformation of cells could involve quantitative and qualitative alteration of integrin function, the effects of EGF on cell-matrix interactions were studied using HSC-1 cells, a human squamous carcinoma cell line showing EGF receptor overexpression. The EGF-treated HSC-1 cells interacted with matrix proteins differently from the untreated cells, as shown by cell adhesion and phagokinetic track assays. Among fibronectin, laminin, fibrinogen, and type I collagen, fibronectin was the most efficient substratum to promote untreated HSC-1 cell adhesion and migration. Pretreatment of the cells with 50 ng/ml EGF for 18 h selectively increased the number of spread cells and the size of the individual cell migration area on type I collagen by 250 and 400%, respectively. The same pretreatment diminished cell adhesion and migration on other substrata so that the EGF treatment converted type I collagen as the most efficient substratum for cell adhesion and migration of the HSC-1 cells. ELISA and immuneprecipitation studies showed that EGF up-regulated the expression of alpha(2) beta(1) integrin collagen receptor in a time- and dose-dependent manner by stimulating biosynthesis of alpha(2) subunit, but did not up-regulate those of the alpha(3) beta(1), alpha(5) beta(1), or alpha(v) beta(3), integrins. These results suggest that EGF preferentially enhances HSC-1 cell interaction with type I collagen, leading to the enhanced cellular migratory activity on the substratum, as a result of selective up-regulation of alpha(2) beta 1( )integrin expression. (C) 1995 Academic Press, Inc.