Anti-apoptotic signaling of the IGF-I receptor in fibroblasts following loss of matrix adhesion

被引：78

作者：

Valentinis, B ^{[1
]}

Morrione, A ^{[1
]}

Peruzzi, F ^{[1
]}

Prisco, M ^{[1
]}

Reiss, K ^{[1
]}

Baserga, R ^{[1
]}

机构：

[1] Thomas Jefferson Univ, Kimmel Canc Ctr, Philadelphia, PA 19107 USA

来源：

ONCOGENE | 1999年 / 18卷 / 10期

关键词：

anchorage-independence; apoptosis; IGI-I receptor; ras; Akt;

D O I：

10.1038/sj.onc.1202471

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The type 1 insulin-like growth factor receptor (IGF-IR) is known to protect cells from a variety of apoptotic injuries. In several instances, the anti-apoptotic effect of the wild type IGF-IR is more evident under conditions of anchorage-independence than in cells in monolayer cultures. We have investigated IGF-IR signaling in cells in anoikis, a form of apoptosis that occurs when cells are denied attachment to the extra-cellular matrix. IGF-I protects mouse embryo fibroblasts (MEF) from anoikis caused by withdrawal of growth factors. Survival is dependent on the concentration of TGF-I and a sufficient number of functional IGF-I receptors. In this model, IGF-I protection correlates best,vith ras activation and cell-to-cell aggregation, while PI3-kinase, Akt and MAP kinases seem to play a lesser, alternative role.

引用

页码：1827 / 1836

页数：10