Resnicoff M, Abraham D, Yutanawiboonchai W, Rotman H L, Kajstura J, Rubin R, Zoltick P, Baserga R
Jefferson Cancer Institute, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
Cancer Res. 1995 Jun 1;55(11):2463-9.
The role of the insulin-like growth factor I receptor (IGF-IR) in programmed cell death has been investigated in vivo in a biodiffusion chamber, where the extent of cell death could be determined quantitatively. We found that a decrease in the number of IGF-IRs causes massive apoptosis in vivo in several transplantable tumors, either from humans or rodents. Conversely, an overexpressed IGF-IR protects cells from apoptosis in vivo. We also show that the same conditions that in vitro cause only partial growth arrest with a minimum of cell death, induce in vivo almost complete cell death. We conclude that the IGF-IR activated by its ligands plays a very important protective role in programmed cell death, and that its protective action is even more striking in vivo than in vitro.
胰岛素样生长因子I受体(IGF-IR)在程序性细胞死亡中的作用已在生物扩散室中进行了体内研究,在该扩散室中可定量确定细胞死亡的程度。我们发现,IGF-IR数量的减少会在体内导致几种可移植肿瘤(无论是人类还是啮齿动物的肿瘤)发生大量凋亡。相反,过度表达的IGF-IR在体内可保护细胞免于凋亡。我们还表明,在体外仅导致部分生长停滞且细胞死亡最少的相同条件,在体内却可诱导几乎完全的细胞死亡。我们得出结论,由其配体激活的IGF-IR在程序性细胞死亡中发挥着非常重要的保护作用,并且其保护作用在体内比在体外更为显著。