Kan O, Baldwin S A, Whetton A D
Department of Biochemistry and Applied Molecular Biology, UMIST, Manchester, United Kingdom.
J Exp Med. 1994 Sep 1;180(3):917-23. doi: 10.1084/jem.180.3.917.
In the absence of a survival stimulus, the interleukin 3 (IL-3)-dependent IC.DP cell line undergoes a process termed programmed cell death or apoptosis. Survival can be induced by IL-3, which can also stimulate proliferation of IC.DP cells. IC.DP cells have been stably transfected with the p160v-abl protein tyrosine kinase, activation of the kinase at the permissive temperature permits cell survival in the absence of IL-3 by suppression of apoptosis, although the growth factor is still required for proliferation. Both IL-3 and activation of the v-ABL tyrosine kinase stimulated glucose transport, which may in part be due to a translocation of transporters to the cell surface. Inhibition of glucose uptake markedly increased the rate of apoptosis in these cells, an effect that could be reversed by the provision of alternative energy sources such as glutamine. Growth factor- or oncogene-mediated increases in glucose uptake may therefore represent an important regulatory point in the suppression of apoptosis.
在缺乏生存刺激的情况下,依赖白细胞介素3(IL-3)的IC.DP细胞系会经历一个被称为程序性细胞死亡或凋亡的过程。IL-3可诱导细胞存活,它还能刺激IC.DP细胞增殖。IC.DP细胞已被稳定转染p160v-abl蛋白酪氨酸激酶,在允许温度下该激酶的激活可通过抑制凋亡使细胞在无IL-3的情况下存活,不过增殖仍需要生长因子。IL-3和v-ABL酪氨酸激酶的激活均刺激葡萄糖转运,这可能部分归因于转运体向细胞表面的转位。抑制葡萄糖摄取显著增加了这些细胞的凋亡率,提供谷氨酰胺等替代能源可逆转这一效应。因此,生长因子或癌基因介导的葡萄糖摄取增加可能是抑制凋亡的一个重要调控点。