CD44 signaling through focal adhesion kinase and its anti-apoptotic effect
CD44 signaling through focal adhesion kinase and its anti-apoptotic effect
复制标题
DOI：
10.1016/s0014-5793(02)03262-3
复制
发表时间：
2002-09-25
期刊：
影响因子：
3.5
通讯作者：
Harigaya, K
中科院分区：
文献类型：
--
作者：
Fujita, Y;Kitagawa, M;Harigaya, K
粘附分子可以启动细胞内信号传导。CD 44通过其天然配体透明质酸或特异性抗体在细胞系上的结合诱导酪氨酸磷酸化和粘着斑激酶（FAK）的激活，然后与磷脂酰肌醇3-激酶（PI 3 K）结合并在其下游激活丝裂原活化蛋白激酶。然而，引入显性负性Rho到细胞中抑制CD 44刺激的FAK磷酸化。表达CD 44的细胞对依托泊苷诱导的凋亡具有显著抵抗性。这种抗凋亡作用被Rho、FAK或PI 3 K的抑制所抵消。这些结果可能表明来自CD 44的信号通路介导了癌细胞对药物诱导的凋亡的抗性。(C)2002年欧洲生物化学学会联合会。由Elsevier Science B. V.出版，版权所有。
Adhesion molecules can initiate intracellular signaling. Engagement of CD44 either by its natural ligand hyaluronan or a specific antibody on a cell line induced tyrosine phosphorylation and activation of focal adhesion kinase (FAK), which then associated with phosphatidylinositol 3-kinase (PI3K) and activated mitogen-activated protein kinase at its downstream. However, the introduction of dominant negative Rho into the cells inhibited the CD44-stimulated FAK phosphorylation. Cells expressing CD44 were significantly resistant to etoposide-induced apoptosis. This anti-apoptotic effect was cancelled by the inhibition of either Rho, FAK or PI3K. These results may indicate a signaling pathway from CD44 to mediate the resistance against drug-induced apoptosis in cancer cells. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.