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首页> 外文期刊>Journal of Cellular Physiology >Regulation of GLUT3 and glucose uptake by the cAMP signalling pathway in the breast cancer cell line ZR-75.
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Regulation of GLUT3 and glucose uptake by the cAMP signalling pathway in the breast cancer cell line ZR-75.

机译：监管GLUT3和葡萄糖吸收的阵营信号通路在乳腺癌细胞系zr - 75。

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Increased glucose uptake as a principal energy source is a requirement for the continued survival of tumour cells. Facilitative glucose transporter-1 (GLUT1) and -3 (GLUT3) have been previously shown to be present and regulated in breast cancer cells and are associated with poor patient prognosis. In cancer cells, the cAMP secondary messenger pathway is known to potentiate described glucose transporter activators and regulate cell fate. However, no regulation of the glucose transporters in breast cancer cells by cAMP has previously been examined. Herein, we determined in the well-characterized breast cancer cell line ZR-75, if the cAMP analogue 8-br-cAMP was capable of regulating GLUT1 and GLUT3 expression and thus glucose uptake. We demonstrated that 8-br-cAMP transiently up-regulates GLUT3 mRNA levels. The use of actinomycin-D and the cloning of 1,200 bp upstream of the human GLUT3 promoter demonstrated that this regulation was transcriptional. Immunocytochemistry and Western blotting confirmed that the increase in mRNA was reflected by an increase in protein levels. No notable regulation of GLUT1 in the presence of 8-br-cAMP was detected. Finally, we determined using the non-metabolizable glucose analogue 2-DOG if this up-regulation in GLUT3 increased glucose uptake. We observed the presence of two uptake components, one corresponding to the Km of GLUT1/4 and the other to GLUT3. A doubling in the uptake velocity was observed only at the Km corresponding to GLUT3. In conclusion, we demonstrate and characterize for the first time, an up-regulation of GLUT3 mRNA, protein and glucose uptake by the cAMP pathway in breast cancer cells.
机译：增加葡萄糖摄取作为主要能源源是一个持续的要求肿瘤细胞的生存。transporter-1 (GLUT1)和3 (GLUT3)以前是现在和监管乳腺癌细胞和与贫困有关病人的预后。二级信使途径是已知的加强了葡萄糖转运体活化剂和调节细胞命运。葡萄糖转运蛋白的调节曾被癌细胞的营地检查。良好的乳腺癌细胞系zr - 75,如果模拟8-br-cAMP营地的能力从而调节GLUT1和GLUT3表达式葡萄糖吸收。瞬变让GLUT3 mRNA水平。利用放线菌素d和1200个基点的克隆人类GLUT3上游启动子本条例是转录。免疫细胞化学和免疫印迹确认mRNA的增加反映通过增加蛋白质含量。监管的GLUT1 8-br-cAMP的存在被检测到。non-metabolizable葡萄糖模拟2-DOG如果这老年病GLUT3增加葡萄糖摄取。我们观察到两个吸收的存在组件,一公里的对应GLUT3 GLUT1/4和其他。吸收速度是观察到的公里对应于GLUT3。首次展示和描述,的老年病GLUT3信使rna,蛋白质和通路在乳腺葡萄糖吸收的营地癌细胞。

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