MiRNA-191 functions as an oncogene in primary glioblastoma by directly targeting NDST1.

小RNA 癌症研究 细胞生长 下调和上调 U87型 胶质瘤 体内 癌基因 生物 胶质母细胞瘤 体外 细胞培养 细胞 基因 细胞周期 生物化学 遗传学
作者
Jinliang Xue,Maosheng Yang,L-H Hua,Z-P Wang
出处
期刊:PubMed 卷期号:23 (14): 6242-6249 被引量:9
标识
DOI:10.26355/eurrev_201907_18443
摘要

Glioblastoma is identified as the most aggressive primary brain tumor. Growing evidence has demonstrated that aberrant expression of miR-191 has oncogenic potentiality in many cancers. However, the effects and the underlying mechanisms of miR-191 in the development of glioblastoma remain largely unknown. The aim of this study was to elucidate the pathobiological functions of miR-191 expression by targeting N-deacetylase/N-sulfotransferase 1 (NDST1) in human glioblastoma.The miR-191 level in human glioblastoma tissues and four cell lines was examined using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Animals study and MTT (3-(4,5-dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay were used to examine the effects of miR-191 on human glioblastoma proliferation. Western blot and Luciferase reporter were used to confirm that miR-191 could regulate NDST1 expression.We found that the miR-191 expression was upregulated in human glioblastoma tissues and cells. MiR-191 over-expression was sufficient to promote human glioblastoma cells growth in vivo and in vitro. We also found that miR-191 directly targeted NDST1 and negatively regulated the NDST1 expression in human glioblastoma cells.In summary, our finding suggested that miR-191 acted as an important regulator in promoting glioblastoma cell proliferation in vivo and in vitro, and this cellular function may be because of its negative regulation of NDST1.

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