Disruption of epithelial cell-matrix interactions induces apoptosis.
Disruption of epithelial cell-matrix interactions induces apoptosis.
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DOI：
10.1083/jcb.124.4.619
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发表时间：
1994-02
期刊：
影响因子：
--
通讯作者：
Francis H
中科院分区：
文献类型：
--
作者：
Frisch SM;Francis H
细胞-基质相互作用对表型特征如基因调控、细胞骨架结构、分化和细胞生长控制方面有重要影响。程序性细胞死亡（凋亡）对于维持适当的细胞数量和组织结构至关重要。因此，确定细胞-基质相互作用是否影响细胞凋亡是有意义的。本报告表明，细胞凋亡是由正常上皮细胞和细胞外基质之间的相互作用的破坏。我们把这种现象称为“失巢”。“bcl-2的过表达保护细胞免受失巢凋亡。细胞对失巢凋亡的敏感性明显受到调节：（a）正常成纤维细胞不发生失巢凋亡;（B）上皮细胞经v-Ha-ras、v-src转化或佛波酯处理后失巢凋亡消失;（c）HT 1080细胞或v-Ha-ras转化的MDCK细胞经腺病毒E1 a逆转后对失巢凋亡敏感;（d）运动因子、分散因子可减轻MDCK细胞的失巢凋亡。结果表明，规避失巢凋亡伴随着收购的锚定独立性或细胞运动。
Cell-matrix interactions have major effects upon phenotypic features such as gene regulation, cytoskeletal structure, differentiation, and aspects of cell growth control. Programmed cell death (apoptosis) is crucial for maintaining appropriate cell number and tissue organization. It was therefore of interest to determine whether cell- matrix interactions affect apoptosis. The present report demonstrates that apoptosis was induced by disruption of the interactions between normal epithelial cells and extracellular matrix. We have termed this phenomenon "anoikis." Overexpression of bcl-2 protected cells against anoikis. Cellular sensitivity to anoikis was apparently regulated: (a) anoikis did not occur in normal fibroblasts; (b) it was abrogated in epithelial cells by transformation with v-Ha-ras, v-src, or treatment with phorbol ester; (c) sensitivity to anoikis was conferred upon HT1080 cells or v-Ha-ras-transformed MDCK cells by reverse- transformation with adenovirus E1a; (d) anoikis in MDCK cells was alleviated by the motility factor, scatter factor. The results suggest that the circumvention of anoikis accompanies the acquisition of anchorage independence or cell motility.