A Mechanism for Regulation of Melanoma Invasion
A Mechanism for Regulation of Melanoma Invasion
复制标题
黑色素瘤侵袭的调节机制
DOI：
--
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发表时间：
1996
影响因子：
4.8
通讯作者：
Wen‐Tien Chen
中科院分区：
文献类型：
--
作者：
H. Nakahara;M. Nomizu;S. K. Akiyama;Yoshihiko Yamada;Y. Yeh;Wen‐Tien Chen
LOX人黑素瘤细胞的侵袭涉及细胞外基质（ECM）降解和细胞表面侵袭伪足的形成。在这里，我们表明，α6β1与来自层粘连蛋白-1 α1链的COOH末端球状结构域的两种肽（层粘连蛋白G肽）（命名为AG-10（NPWHSIYITRFG）和AG-32（TWYKIAFQRNRK））以及针对α6和β1整联蛋白的抗体的连接促进了侵袭性。AG-10和AG-32抑制层粘连蛋白上的细胞粘附，并且抗体阻断固定的AG-10和AG-32上的细胞粘附，表明肽主要与α6β1整联蛋白相互作用。这些可溶性肽和整联蛋白抗体通过引起ECM降解和侵袭足活性的2-3倍增加而诱导侵袭性，所述侵袭足活性独立于与ECM预结合的整联蛋白的粘附活性。诱导的ECM降解和侵袭与170 kDa膜结合明胶酶，seprase，以及其强烈的本地化在invadopodia，但不是在焦点粘连的表面表达增加。然而，seprase、明胶酶A和β1整合素的总表达水平没有改变。我们认为，层粘连蛋白G肽通过刺激侵袭伪足活性作用于α6β1整合素信号传导，这与它们对固定化ECM上细胞粘附的直接作用不同。
Invasion of LOX human melanoma cells involves extracellular matrix (ECM) degradation and formation of cell surface invadopodia. Here we show that the ligation of α6β1 by two peptides derived from the COOH-terminal globular domain of laminin-1 α1 chain (laminin G peptides), designated AG-10 (NPWHSIYITRFG) and AG-32 (TWYKIAFQRNRK), and antibodies against α6 and β1 integrins promoted invasiveness. AG-10 and AG-32 inhibited cell adhesion on laminin, and the antibodies blocked cell adhesion on immobilized AG-10 and AG-32, suggesting that the peptides interact primarily with α6β1 integrin. These soluble peptides and integrin antibodies induced invasiveness by causing an 2-3-fold increase in ECM degradation and invadopodial activity independently of adhesion activity of integrins that were prebound to ECM. The induced ECM degradation and invasion was associated with an increased surface expression of the 170-kDa membrane-bound gelatinase, seprase, as well as its intense localization at invadopodia but not at focal adhesions. However, the total expression levels of seprase, gelatinase A and β1 integrins were not altered. We suggest that laminin G peptides act on the α6β1 integrin signaling of invasion by stimulating invadopodial activities, which is distinct from their direct effects on cell adhesion on immobilized ECM.
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DOI：
10.1073/pnas.88.19.8392
发表时间：
1991-10-01
影响因子：
11.1
作者：
KORNBERG, LJ;EARP, HS;JULIANO, RL
通讯作者：
JULIANO, RL
DOI：
10.1016/s0021-9258(18)35853-8
发表时间：
1992-11
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
L. Kornberg;H. Earp;J. Parsons;M. D. Schaller;Rudy L. Juliano
通讯作者：
L. Kornberg;H. Earp;J. Parsons;M. D. Schaller;Rudy L. Juliano
影响因子：
11.2
作者：
R. E. Seftor;E. Seftor;W. Stetler-Stevenson;M. Hendrix
通讯作者：
R. E. Seftor;E. Seftor;W. Stetler-Stevenson;M. Hendrix
细胞侵入基质珠：β1 整合素和纤连蛋白定位于侵入伪足。
影响因子：
4
作者：
Mueller,SC;Chen,WT
通讯作者：
Chen,WT
通过层粘连蛋白 A 链衍生的合成肽调节小鼠 B16F10 黑色素瘤纤溶酶原激活剂的产生。
影响因子：
11.2
作者：
Stack,MS;Gray,RD;Pizzo,SV
通讯作者：
Pizzo,SV