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NCBP3/SNHG6 inhibits GBX2 transcription in a histone modification manner to facilitate the malignant biological behaviour of glioma cells.
RNA Biology ( IF 3.6 ) Pub Date : 2020-07-26 , DOI: 10.1080/15476286.2020.1790140
Xiwen Li 1, 2, 3 , Fangfang Zhang 1, 2, 3 , Jun Ma 1, 2, 3 , Xuelei Ruan 1, 2, 3 , Xiaobai Liu 4, 5, 6 , Jian Zheng 4, 5, 6 , Yunhui Liu 4, 5, 6 , Shuo Cao 1, 2, 3 , Shuyuan Shen 1, 2, 3 , Lianqi Shao 1, 2, 3 , Heng Cai 4, 5, 6 , Zhen Li 4, 5, 6 , Yixue Xue 1, 2, 3
Affiliation  

ABSTRACT

RNA-binding proteins (RBPs) are significantly dysregulated in glioma. In this study, we demonstrated the upregulation of Nuclear cap-binding subunit 3 (NCBP3) in glioma tissues and cells. Further, knockdown of NCBP3 inhibited the malignant progression of glioma. NCBP3 directly bound to small nucleolar RNA host gene 6 (SNHG6) and stabilized SNHG6 expression. In contrast, the gastrulation brain homeobox 2 (GBX2) transcription factor was downregulated in glioma tissues and cells. SNHG6 inhibited GBX2 transcription by mediating the H3K27me3 modification induced by polycomb repressive complex 2 (PRC2). Moreover, GBX2 decreased the promoter activities and downregulated the expression of the flotillin protein family 1 (FLOT1) oncogene. In conclusion, NCBP3/SNHG6 inhibits GBX2 transcription in a PRC2-dependent manner to facilitate the malignant progression of gliomas.



中文翻译:

NCBP3/SNHG6 以组蛋白修饰的方式抑制 GBX2 转录,促进胶质瘤细胞的恶性生物学行为。

摘要

RNA 结合蛋白 (RBP) 在神经胶质瘤中显着失调。在这项研究中,我们证明了神经胶质瘤组织和细胞中核帽结合亚基 3 (NCBP3) 的上调。此外,NCBP3 的敲低抑制了胶质瘤的恶性进展。NCBP3 直接结合小核仁 RNA 宿主基因 6 (SNHG6) 并稳定 SNHG6 表达。相比之下,原肠胚形成大脑同源盒 2 (GBX2) 转录因子在神经胶质瘤组织和细胞中被下调。SNHG6 通过介导多梳抑制复合物 2 (PRC2) 诱导的 H3K27me3 修饰来抑制 GBX2 转录。此外,GBX2 降低启动子活性并下调 flotillin 蛋白家族 1 (FLOT1) 癌基因的表达。综上所述,

更新日期:2020-07-26
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