Study of global transcriptional changes of N-GlcNAc2 proteins-producing T24 bladder carcinoma cells under glucose deprivation.
Study of global transcriptional changes of N-GlcNAc2 proteins-producing T24 bladder carcinoma cells under glucose deprivation.
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DOI：
10.1371/journal.pone.0060397
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Suzaki M
中科院分区：
文献类型：
--
作者：
Isono T;Chano T;Okabe H;Suzaki M
已认识到N-连接（β-N-乙酰葡糖胺）2 [N-GlcNAc 2]-修饰蛋白水平的增加是对葡萄糖剥夺的有效应答。在本研究的第一步中，使用下一代测序仪，我们研究了T24膀胱癌细胞系中葡萄糖剥夺诱导的全局转录变化，在葡萄糖剥夺下产生N-GlcNAc 2修饰的蛋白。我们的转录组分析显示UDP-GlcNAc生物合成途径和未折叠蛋白反应基因的显著上调，以及含有有丝分裂激酶的G2/M转换相关基因的下调。我们的生物学分析证实，N-GlcNAc 2修饰的蛋白质与ER中的BiP蛋白一起定位。G2/M期阻滞由葡萄糖剥夺引起。此外，未折叠蛋白反应基因的敲低诱导有丝分裂激酶在葡萄糖剥夺下的表达恢复。两者合计，我们的研究结果表明，N-GlcNAc 2修饰的蛋白质产生葡萄糖剥夺引起的未折叠的蛋白质反应在ER中，这种反应诱导G2/M期阻滞。
Increased levels of N-linked (β-N- acetylglucosamine)2 [N-GlcNAc2]-modified proteins have been recognized to be an effective response to glucose deprivation. In the first step of this study, using a next generation sequencer, we investigated the global transcriptional changes induced by glucose deprivation in a T24 bladder carcinoma cell line, producing N-GlcNAc2-modified proteins under glucose deprivation. Our transcriptome analysis revealed significant up-regulation of the UDP-GlcNAc biosynthesis pathway and unfolded protein response genes, and down-regulation of G2/M transition-related genes containing mitotic kinases. Our biological analysis confirmed that N-GlcNAc2-modified proteins were localized with BiP proteins in the ER. G2/M arrest was caused by glucose deprivation in T24 cells. Moreover, the knockdown of unfolded protein response genes induced the expressional recovery of mitotic kinases under glucose deprivation. Taken together, our results suggest N-GlcNAc2-modified proteins produced under glucose deprivation caused unfolded protein response in the ER, and that this response induced G2/M arrest.
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