Differential activation of ERKs to focal adhesions by PKC ε is required for PMA-induced adhesion and migration of human glioma cells
Differential activation of ERKs to focal adhesions by PKC ε is required for PMA-induced adhesion and migration of human glioma cells
复制标题
DOI：
10.1038/sj.onc.1204899
复制
发表时间：
2001-11-01
期刊：
影响因子：
8
通讯作者：
Yong, VW
中科院分区：
文献类型：
--
作者：
Besson, A;Davy, A;Yong, VW
蛋白激酶C(PKC)是。丝氨酸/苏氨酸激酶家族。牵涉到。各种信号的传递。越来越多的证据表明，特定的PKC亚型参与调节不同的细胞过程。在胶质瘤细胞中，PKCα被发现是细胞增殖和细胞周期进程的关键调节因子，白色PKC epsilon被发现调节黏附和迁移。在这里，我们。有报道称，特定的PKC亚型能够不同地激活细胞外信号调节激酶(ERK)！在不同的细胞位置：当PKCα诱导核内ERK的激活时，PKC epsilon诱导ERK的激活，而ERK在局部粘连处激活。抑制ERK通路可完全消除PKC诱导的整合素介导的黏附和迁移。因此，我们首次提出证据表明，PKC epsilon能够在局部粘连处激活ERK，以介导胶质瘤细胞的黏附和运动，提供了一种分子机制。解释PKCα和epsilon在胶质瘤细胞中的不同生物学功能。
Protein kinase C (PKC) is. a family of serine/threonine kinases. involved in. the transduction of a variety of signals. There is increasing evidence to indicate that specific PKC isoforms are involved in the regulation of distinct cellular processes. In glioma, cells, PKC alpha was found to be a critical regulator of proliferation and cell cycle progression, white PKC epsilon was found to regulate adhesion and migration. Herein, we. report that specific PKC isoforms are able to differentially activate extracellular-signal regulated kinase (ERK)! in distinct cellular locations: while PKC alpha induces the activation of nuclear ERK, PKC epsilon induces, the activation of ERK at focal adhesions. Inhibition of the ERK pathway completely abolished the PKC-induced integrin-mediated adhesion and migration. Thus, we present the first evidence that PKC epsilon is able to, activate ERK at focal adhesions to mediate glioma cell adhesion and motility, providing a molecular mechanism to. explain the different biological functions of PKC alpha and epsilon in glioma cells.