Long non-coding RNA CASP5 promotes the malignant phenotypes of human glioblastoma multiforme

被引:18
|
作者
Zhou, Yali [1 ]
Dai, Wei [2 ]
Wang, Handong [1 ]
Pan, Hao [1 ]
Wang, Qiang [1 ]
机构
[1] Nanjing Univ, Sch Med, Jinling Hosp, Dept Neurosurg, 305 East Zhongshan Rd, Nanjing 210002, Jiangsu, Peoples R China
[2] Nanjing Med Univ, Sch Med, Jinling Hosp, Dept Neurosurg, Nanjing 210002, Jiangsu, Peoples R China
基金
中国博士后科学基金; 中国国家自然科学基金;
关键词
GBM; IncRNA; Proliferation; Invasion; CANCER; DISEASE; FRONTIER; SYSTEM;
D O I
10.1016/j.bbrc.2018.04.217
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background. Long non-coding RNAs (IncRNAs) have been demonstrated to be intensively involved in the development of various carcinomas, including glioblastoma multiforme (GBM). However, only a few of them have been well characterized. LncRNA CASP5 have been found to be up-regulated in GBM tissues compared with normal tissues in a microarray-based IncRNA profiling study. In the present study, we further explored the biological role of IncRNA CASP5 in GBM Methods. We examined the expression level of IncRNA CASP5 in GBM tissues as well as GBM cell lines. CCK-8 assay, flow cytometric analysis, western blotting, orthotopic GBM model as well as transwell assay were performed to investigate the biological role of CASP5. Results. We observed that IncRNA CASP5 was highly expressed in GBM tissues and cell lines. Knockdown of CASP5 greatly inhibited GBM proliferation and resulted in G1 cell cycle arrest along with higher apoptosis ratios in vitro and in vivo, while overexpression led to the opposite phenomenon Furthermore, the migration and invasion ability of GBM cells were significantly decreased after CASP5 downregulation, while increased migration and invasion can be observed after CASP5 up-regulation. Conclusion We demonstrate for the first time the potential oncogenic role of IncRNA CASP5 which may be helpful for identifying novel therapeutic targets in GBM (C) 2018 Elsevier Inc. All rights reserved.
引用
收藏
页码:966 / 972
页数:7
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