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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。
Objective: To investigate the effect of NDRG2 on the histone acetylation of glioma U87-MG cells, to clarify the mechanism of its anti-tumor from the perspective of metabolomics and to provide new ideas for the treatment of glioma. Methods: The lentivirus-mediated exogenous NDRG2 gene was overexpressed in glioma U87-MG cell line and the effect of lentivirus on the proliferation of glioma U87-MG cells was detected by MTT assay. Acetyl histone acetylation and phosphorylation status of AKT-ACLY pathway in glioma U87-MG cells were detected. The intracellular acetyl-CoA level was detected by enzyme-linked reaction. Results: Overexpression of NDRG2 in glioma U87-MG cells decreased the phosphorylation of AKT and ACLY, reduced the intracellular acetyl-CoA synthesis and inhibited the histone acetylation. Conclusion: NDRG2 may inhibit the proliferation of glioma U87-MG cells by inhibiting AKT pathway and decreasing histone acetylation.