急性l -谷氨酰胺剥夺影响U87胶质瘤细胞中tp53相关蛋白基因的表达。

D. Minchenko, S. V. Danilovskyi, I. V. Kryvdiuk, N. A. Hlushchak, O. V. Kovalevska, L. L. Karbovskyi, O. Minchenko
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引用次数: 9

摘要

我们研究了急性l -谷氨酰胺剥夺对肿瘤蛋白53 (TP53)相关基因如TOPORS(拓扑异构酶I结合、富含精氨酸/丝氨酸、E3泛素蛋白连接酶)、TP53BPI (TP53结合蛋白1)、TP53TG1 (TP53诱导基因1)、SESN1 (p53调节的pa26核蛋白)、NME6 (NME/NM23核苷二磷酸激酶6)和ZMAT3(锌指基质型3)在ERN1敲低的胶质瘤细胞中的表达的影响。结果表明,在U87胶质瘤细胞中,阻断ERN1功能可诱导RYBP和SESN1基因的表达,而抑制TP53BP1、TP53TG1、TOPORS、NME6等基因的表达。此外,在l -谷氨酰胺剥夺条件下,rybpi SESN1、TP53BP1和ZMAT3基因的表达水平在对照胶质瘤细胞中增加,但阻断ERN1信号酶功能可显著增强对所有这些基因表达的影响。同时,ERN1敲低消除了TP53TG1和TOPORS基因对l -谷氨酰胺剥夺条件的反应。本研究结果清楚地表明,大多数编码tp53相关因子的基因的表达依赖于急性l -谷氨酰胺剥夺状态以及内质网应激的主要信号系统ERN1。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Acute L-glutamine deprivation affects the expression of TP53-related protein genes in U87 glioma cells.
We have studied the effect of acute L-glutamine deprivation on the expression oftumor protein 53 (TP53)-related genes such as TOPORS (topoisomerase I binding, arginine/serine-rich, E3 ubiquitin protein ligase), TP53BPI (TP53 bindingprotein 1), TP53TG1 (TP53 inducible gene 1), SESN1 (p53 regulatedPA26 nuclear protein), NME6 (NME/NM23 nucleoside diphosphate kinase 6), and ZMAT3 (zinc finger Matrin-type 3) in glioma cells with ERN1 knockdown. It was shown that blockade of ERN1 finction in U87 glioma cells is induced the expression of RYBP and SESN1 genes, but decreased the expression of TP53BP1, TP53TG1, TOPORS, NME6, genes. Moreover, the expression levels ofRYBPI SESN1, TP53BP1, and ZMAT3 genes is increased in control glioma cells by L-glutamine deprivation condition but blockade of ERN1 signaling enzyme function significantly enhances this effect on the expression all of these genes. At the same time, the ERN1 knockdown eliminates the response TP53TG1 and TOPORS genes to L-glutamine deprivation condition. Results of this investigation clearly demonstrate that the expression most of genes encoding TP53-related factors depends upon acute L-glutamine deprivation condition as well as upon ERN1, the major signaling system of the endoplasmic reticulum stress.
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