Article Summary
葛英为,秦 娜,于修贤,白文红,邓艳春.NDRG2对胶质瘤U87-MG细胞组蛋白乙酰化的影响及机制研究[J].现代生物医学进展英文版,2017,17(13):2431-2434.
NDRG2对胶质瘤U87-MG细胞组蛋白乙酰化的影响及机制研究
The Effect and Mechanism of NDRG2 on the Histone Acetylation of Glioma U87-MG Cells
Received:December 03, 2016  Revised:December 26, 2016
DOI:10.13241/j.cnki.pmb.2017.13.008
中文关键词: 胶质瘤  组蛋白  乙酰化  NDRG2  细胞增殖  柠檬酸裂解酶
英文关键词: Glioma  Histone  Acetylation  NDRG2  Proliferation  ATP-Citrate lyase
基金项目:陕西省自然科学基金项目(2014JM3080)
Author NameAffiliationE-mail
葛英为 第四军医大学西京医院神经内科 陕西 西安 710032 aspirins@live.cn 
秦 娜 第四军医大学西京医院神经内科 陕西 西安 710032  
于修贤 第四军医大学西京医院神经内科 陕西 西安 710032  
白文红 第四军医大学西京医院神经内科 陕西 西安 710032  
邓艳春 第四军医大学西京医院神经内科 陕西 西安 710032  
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中文摘要:
      摘要 目的:探讨NDRG2对胶质瘤U87-MG细胞组蛋白乙酰化的影响,从代谢组学角度明确其抑癌机制,为胶质瘤治疗提供新思路。方法:利用慢病毒介导的外源性NDRG2基因在胶质瘤U87-MG细胞株中过表达,并采用MTT检测其对胶质瘤U87-MG细胞增殖的影响,采用Western blot技术研究其对胶质瘤U87-MG细胞组蛋白乙酰化及AKT-ACLY通路磷酸化状态的影响,并使用酶联反应检测胞内乙酰辅酶A的水平。结果:NDRG2在胶质瘤U87-MG细胞中外源过表达可降低AKT及下游分子ACLY的磷酸化水平,减少胞内乙酰辅酶A的合成,抑制组蛋白乙酰化。结论:NDRG2可能通过抑制AKT通路,减少组蛋白乙酰化,进而抑制胶质瘤U87-MG细胞增殖。
英文摘要:
      ABSTRACT Objective: To explore the effect and mechanism of NDRG2 on the histone acetylation in U87-MG cells and provide new ideas for the treatment of glioma. Methods: NDRG2 overexpression was mediated by lentivirus, and the level of histone acetylation was measured by Western blot using acetylation antibodies in U87-MG cells. ELISA was used to evaluated the effect on acetyl-CoA metabolism of NDRG2 overexpression. The AKT-ACLY pathway was detected to illustrated this mechanism. Results: The phosphoryla- tion of AKT and ACLY in U87MG cell were significantly down-regulated with the overexpression of NDRG2, resulting in change of acetyl-CoA/CoA ratio. The histone acetylation level was down-regulated, which had an effect on the proliferation of glioma cells. Conclusion: NDRG2 might participate in the metabolism of acetyl-CoA and regulate the histone acetylation, which could further suppress the proliferation of U87-MG glioma cell.
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