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Specific protein 1 depletion attenuates glucose uptake and proliferation of human glioma cells by regulating GLUT3 expression

机译:特定蛋白1的消耗通过调节GLUT3的表达来减弱人胶质瘤细胞的葡萄糖摄取和增殖

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摘要

It has been reported previously that the expression of glucose transporter member 3 (GLUT3) is increased in malignant glioma cells compared with normal filial cells. However, the regulating mechanism that causes this phenomenon remains unknown. The present study investigated the regulating role of transcription factor specific protein 1 (Sp1) in GLUT3 expression in a human glioma cell line. In the present study, Sp1 was identified to directly bind to the GLUT3 3-untranslated region in human glioma U251 cells. Small interfering RNA- and the Sp1-inhibitor mithramycin.A-mediated Sp1 knockdown experiments revealed that Spl depletion decreased glucose uptake and inhibited cell growth and invasion of 1.3251 cells by downregulating GLUT3 expression. Therefore SO is an important positive regulator for the expression of GLUT3 in human glioma cells, and may explain the overexpression of GLUT3 in U251 cells. These results suggest that Spl may have a role in glioma treatment.
机译:先前已有报道,与正常的孝子细胞相比,恶性神经胶质瘤细胞中葡萄糖转运蛋白3(GLUT3)的表达增加。但是,导致这种现象的调节机制仍然未知。本研究调查了转录因子特异性蛋白1(Sp1)在人胶质瘤细胞系中GLUT3表达中的调节作用。在本研究中,Sp1被鉴定为与人神经胶质瘤U251细胞中的GLUT3 3非翻译区直接结合。小干扰RNA和Sp1抑制剂的光神霉素。A介导的Sp1敲低实验表明,Spl耗竭通过下调GLUT3的表达降低了葡萄糖的摄取并抑制了1.3251细胞的生长和侵袭。因此,SO是人胶质瘤细胞中GLUT3表达的重要正调节剂,并可能解释GLUT3在U251细胞中的过表达。这些结果表明,Spl可能在神经胶质瘤治疗中起作用。

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