Regulation of glucose transport by interleukin-3 in growth factor-dependent and oncogene-transformed bone marrow-derived cell lines

Regulation of glucose transport by interleukin-3 in growth factor-dependent and oncogene-transformed bone marrow-derived cell lines
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DOI:
10.1016/s0145-2126(97)00016-7
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发表时间:
1997-07-01
期刊:
影响因子:
2.7
通讯作者:
Berridge, MV
Berridge, MV
中科院分区:
医学3区
文献类型:
--
作者:
Ahmed, N;Berridge, MV

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生长因子通过刺激葡萄糖向细胞内的运输和在细胞周期中推进细胞来维持细胞的活力和促进细胞的生长。在短期内,对葡萄糖运输的影响涉及转运体的激活,而从长期来看,涉及基因表达的增加。本研究旨在研究生长因子对白介素3依赖的骨髓源性细胞系及其癌基因转化细胞系葡萄糖转运的调节作用。将32D克隆3(32Dcl3)细胞和温敏性(Ts)RES和abl癌基因转染的细胞分别用IL-3和不加IL-3处理,比较它们摄取2-脱氧-D-葡萄糖的能力。在32摄氏度的允许温度下,不依赖IL-3生长的转化细胞表现出比IL-3最佳刺激的对照细胞高2到6倍的增殖反应、增强的酪氨酸激酶活性和c-myc表达。与对照32DCl3细胞相比,转化细胞对P-脱氧-D-葡萄糖的摄取量也提高了36-76%。转化细胞葡萄糖摄取量的增加与葡萄糖转运体对葡萄糖的亲和力提高了2.5倍是一致的。IL-3促进对照细胞和癌基因转化细胞的葡萄糖摄取。在对照和RES转化的细胞中,IL-3响应的葡萄糖摄取增加与葡萄糖转运体对葡萄糖的亲和力增加有关,但在ABL转化的细胞中,亲和力没有明显的变化。IL-3还增加了对照细胞和癌基因转化细胞中葡萄糖转运体的表达,这表明转运体表达的增加以及转运体对葡萄糖亲和力的变化可以影响葡萄糖的摄取。(C)1997年爱思唯尔科学有限公司。
Growth factors maintain cell viability and promote cell growth by stimulating glucose transport into cells and by progressing cells through the cell cycle. In the short term, effects on glucose transport involve transporter activation, while in the longer term increased gene expression is involved. This study aimed to investigate growth factor regulation of glucose transport in an interleukin (IL)-3-dependent bone marrow-derived cell line and its oncogene-transformed counterparts. 32D clone 3 (32Dcl3) cells and cells transfected with temperature-sensitive (ts) res and abl oncogenes, were treated with and without IL-3 and their ability to take up 2-deoxy-D-glucose compared. Transformed cells, which are not dependent on IL-3 for growth at the permissive temperature of 32 degrees C, exhibited a two-to six-fold higher proliferative response, enhanced tyrosine kinase activity and c-myc expression than control cells optimally stimulated with IL-3. Compared with control 32Dcl3 cells, P-deoxy-D-glucose uptake was also 36-76% higher in transformed cells. The increased glucose uptake in transformed cells was consistent with 2.5-fold higher affinity of the glucose transporters for glucose. IL-3 stimulated glucose uptake in both control and oncogene-transformed cells. With control and res-transformed cells, enhanced glucose uptake in response to IL-3 was associated with increased affinity of glucose transporters for glucose but with abl-transformed cells, no significant affinity changes were observed. IL-3 also increased glucose transporter expression in both control and oncogene-transformed cells, suggesting that increased transporter expression as well as changes in transporter affinity for glucose can affect glucose uptake. (C) 1997 Elsevier Science Ltd.