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miR-136 通过靶向 AEG-1 和 Bcl-2 促进神经胶质瘤细胞凋亡。

MiR-136 promotes apoptosis of glioma cells by targeting AEG-1 and Bcl-2.

机构信息

Key Laboratory of Tropical Disease Control, Sun Yat-Sen University, Ministry of Education, Guangzhou, Guangdong, China.

出版信息

FEBS Lett. 2012 Oct 19;586(20):3608-12. doi: 10.1016/j.febslet.2012.08.003. Epub 2012 Aug 9.

Abstract

MicroRNAs have the capacity to coordinately repress multiple target genes and interfere with biological functions of the cell, such as proliferation and apoptosis. Here we report that miR-136 is downregulated in human glioma, and that the miRNA promotes apoptosis of glioma cells induced by chemotherapy. Two anti-apoptotic genes, AEG-1 and Bcl-2, are identified as targets of miR-136, and restoration of AEG-1 or Bcl-2 expression suppresses miR-136-enhanced apoptosis. Therefore, miR-136 might play a tumor-suppressive role in human glioma and thereby might represent a potential therapeutic strategy.

摘要

微小 RNA 能够协调抑制多个靶基因,并干扰细胞的生物学功能,如增殖和凋亡。在这里,我们报告 miR-136 在人神经胶质瘤中下调,并且 miRNA 促进化疗诱导的神经胶质瘤细胞凋亡。两个抗凋亡基因,AEG-1 和 Bcl-2,被鉴定为 miR-136 的靶基因,并且 AEG-1 或 Bcl-2 的表达恢复抑制 miR-136 增强的凋亡。因此,miR-136 可能在人神经胶质瘤中发挥肿瘤抑制作用,因此可能代表一种潜在的治疗策略。

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