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首页> 外文期刊>Neuropathology and applied neurobiology >Enhancer of Zeste 2 (EZH2) is up-regulated in malignant gliomas and in glioma stem-like cells.
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Enhancer of Zeste 2 (EZH2) is up-regulated in malignant gliomas and in glioma stem-like cells.

机译：Zeste 2（EZH2）的增强剂在恶性神经胶质瘤和神经胶质瘤干样细胞中被上调。

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F. Orzan, S. Pellegatta, P. L. Poliani, F. Pisati, V. Caldera, F. Menghi, D. Kapetis, C. Marras, D. Schiffer and G. Finocchiaro (2011) Neuropathology and Applied Neurobiology37, 381-394 Enhancer of Zeste 2 (EZH2) is up-regulated in malignant gliomas and in glioma stem-like cells Aims: Proteins of the Polycomb repressive complex 2 (PRC2) are epigenetic gene silencers and are involved in tumour development. Their oncogenic function might be associated with their role in stem cell maintenance. The histone methyltransferase Enhancer of Zeste 2 (EZH2) is a key member of PRC2 function: we have investigated its expression and function in gliomas. Methods:EZH2 expression was studied in grade II-IV gliomas and in glioma stem-like cells (GSC) by quantitative PCR and immunohistochemistry. Effects of EZH2 down-regulation were analysed by treating GSC with the histone deacetylase (HDAC) inhibitor suberoylanide hydroxamic acid (SAHA) and by shRNA. Results: DNA microarray analysis showed that EZH2 is highly expressed in murine and human GSC. Real-time PCR on gliomas of different grade (n = 66) indicated that EZH2 is more expressed in glioblastoma multiforme (GBM) than in low-grade gliomas (P = 0.0013). This was confirmed by immunohistochemistry on an independent set of 106 gliomas. Treatment with SAHA caused significant up-regulation of PRC2 predicted target genes, GSC disruption and decreased expression of EZH2 and of the stem cell marker CD133. Inhibition of EZH2 expression by shRNA was associated with a significant decrease of glioma proliferation. Conclusion: The data suggest that EZH2 plays a role in glioma progression and encourage the therapeutic targeting of these malignancies by HDAC inhibitors.
机译：F.Orzan，S.Pellegatta，PL Poliani，F.Pisati，V.Caldera，F.Menghi，D.Kapetis，C.Marras，D.Schiffer和G.Finocchiaro（2011）神经病理学和应用神经生物学37，381-394 Enhancer Zeste 2（EZH2）的表达在恶性神经胶质瘤和神经胶质瘤干样细胞中被上调。目的：聚梳抑制复合物2（PRC2）的蛋白质是表观遗传基因沉默子，参与肿瘤的发展。它们的致癌功能可能与其在干细胞维持中的作用有关。 Zeste 2（EZH2）的组蛋白甲基转移酶增强子是PRC2功能的关键成员：我们已经研究了它在神经胶质瘤中的表达和功能。方法：通过定量PCR和免疫组化方法研究II-IV级神经胶质瘤和神经胶质瘤干样细胞（GSC）中EZH2的表达。通过用组蛋白脱乙酰基酶（HDAC）抑制剂次木聚糖异羟肟酸（SAHA）处理GSC和shRNA来分析EZH2下调的作用。结果：DNA芯片分析表明EZH2在鼠和人GSC中高表达。实时PCR对不同级别（n = 66）的神经胶质瘤的研究表明，EZH2在多形性胶质母细胞瘤（GBM）中的表达高于低度神经胶质瘤（P = 0.0013）。通过免疫组化对独立的106个神经胶质瘤进行了证实。 SAHA处理导致PRC2预测的靶基因显着上调，GSC破坏以及EZH2和干细胞标记CD133的表达降低。 shRNA抑制EZH2表达与神经胶质瘤增殖的显着降低有关。结论：数据表明，EZH2在神经胶质瘤进展中发挥作用，并通过HDAC抑制剂促进治疗性靶向这些恶性肿瘤。

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