焦点粘着
细胞迁移
细胞生物学
卡尔帕因
钙蛋白酶抑制剂
细胞粘附
半胱氨酸蛋白酶8
半胱氨酸蛋白酶3
转移
细胞凋亡
半胱氨酸蛋白酶
癌症研究
生物
细胞
化学
程序性细胞死亡
信号转导
生物化学
癌症
酶
遗传学
作者
Simone Barbero,Ainhoa Mielgo,Vicente A. Torres,Tal Teitz,David J. Shields,David Mikolon,Matthew Bogyo,Daniela Barilà,Jill M. Lahti,David D. Schlaepfer,Dwayne G. Stupack
出处
期刊:Cancer Research
[American Association for Cancer Research]
日期:2009-04-22
卷期号:69 (9): 3755-3763
被引量:132
标识
DOI:10.1158/0008-5472.can-08-3937
摘要
Caspase-8 is a proapoptotic protease that suppresses neuroblastoma metastasis by inducing programmed cell death. Paradoxically, caspase-8 can also promote cell migration among nonapoptotic cells; here, we show that caspase-8 can promote metastasis when apoptosis is compromised. Migration is enhanced by caspase-8 recruitment to the cellular migration machinery following integrin ligation. Caspase-8 catalytic activity is not required for caspase-8-enhanced cell migration; rather, caspase-8 interacts with a multiprotein complex that can include focal adhesion kinase and calpain 2 (CPN2), enhancing cleavage of focal adhesion substrates and cell migration. Caspase-8 association with CPN2/calpastatin disrupts calpastatin-mediated inhibition of CPN2. In vivo, knockdown of either caspase-8 or CPN2 disrupts metastasis among apoptosis-resistant tumors. This unexpected molecular collaboration provides an explanation for the continued or elevated expression of caspase-8 observed in many tumors.
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