Frisch S M, Ruoslahti E
Burnham Institute, La Jolla Cancer Research Center, CA 92037, USA.
Curr Opin Cell Biol. 1997 Oct;9(5):701-6. doi: 10.1016/s0955-0674(97)80124-x.
The loss of integrin-mediated cell-matrix contact induces apoptosis ('anoikis') in certain cell types. Recently it has been shown that protein kinase signaling pathways control anoikis both positively and negatively. Focal adhesion kinase, when activated by integrins, can suppress anoikis. Phosphatidylinositol 3-kinase and the AKT oncoprotein may mediate the anoikis-suppressing effects of focal adhesion kinase. Conversely, the stress-activated protein kinase/Jun amino-terminal kinase pathway promotes anoikis. Latest results indicate that caspase-mediated cleavage of the first component of this latter pathway, MEKK-1, may trigger activation of this pathway in anoikis. In addition, certain integrins may regulate bcl-2 expression levels, possibly adjusting the threshold for anoikis.
整合素介导的细胞与基质接触的丧失会在某些细胞类型中诱导凋亡(“失巢凋亡”)。最近的研究表明,蛋白激酶信号通路对失巢凋亡具有正向和负向调控作用。黏着斑激酶在被整合素激活后,可以抑制失巢凋亡。磷脂酰肌醇3激酶和AKT癌蛋白可能介导黏着斑激酶的失巢凋亡抑制作用。相反,应激激活蛋白激酶/ Jun氨基末端激酶通路则促进失巢凋亡。最新研究结果表明,半胱天冬酶介导的该通路首个组分MEKK-1的裂解可能会在失巢凋亡过程中触发该通路的激活。此外,某些整合素可能会调节bcl-2的表达水平,从而可能调整失巢凋亡的阈值。