Knockdown of long non-coding RNA ANRIL inhibits proliferation, migration, and invasion but promotes apoptosis of human glioma cells by upregulation of miR-34a

2017 ◽  
Vol 119 (3) ◽  
pp. 2708-2718 ◽  
Author(s):  
Xuechao Dong ◽  
Zheng Jin ◽  
Yong Chen ◽  
Haiyang Xu ◽  
Chengyuan Ma ◽  
...  
IUBMB Life ◽  
2018 ◽  
Vol 71 (1) ◽  
pp. 93-104 ◽  
Author(s):  
Qi Wang ◽  
Zhong-Wei Zhuang ◽  
Yi-Ming Cheng ◽  
Ji-Qiang Ma ◽  
Shi-Yi Xu ◽  
...  

2017 ◽  
Vol 37 (6) ◽  
Author(s):  
Anqiang Yang ◽  
Handong Wang ◽  
Xiaobing Yang

Human glioma is one of the malignant tumors of the central nervous system (CNS). Its prognosis is poor, which is due to its genetic heterogeneity and our poor understanding of its underlying molecular mechanisms. The present study aimed to assess the relationship between plasmacytoma variant translocation 1 (PVT1) and enhancer of zeste homolog 2 (EZH2), and their effects on the proliferation and invasion of glioma cells. The expression levels of PVT1 and EZH2 in human glioma tissues and cell lines were measured using quantitative RT-PCR (qRT-PCR). Then, after siRNA-PVT1 and entire PVT1 sequence vector transfection, we determined the regulation roles of PVT1 in the proliferation, apoptosis, migration, and invasion of glioma cells. We found that the expression levels of both PVT1 and EZH2 were up-regulated in human glioma tissues and cell lines, and positively correlated with glioma malignancy. And, silencing of PVT1 expression resulted in decreased proliferation, increased apoptosis, and decreased migration and invasion. In addition, exogenous PVT1 led to increased EZH2 expression and increased proliferation and induced proliferation and invasion. These data inferred that long non-coding RNA PVT1 could be served as an indicator of glioma prognosis, and PVT1–EZH2 regulatory pathway may be a novel therapeutic target for treating glioma.


Oncotarget ◽  
2015 ◽  
Vol 6 (26) ◽  
pp. 21934-21949 ◽  
Author(s):  
Jing Ke ◽  
Yi-long Yao ◽  
Jian Zheng ◽  
Ping Wang ◽  
Yun-hui Liu ◽  
...  

Author(s):  
Junfeng Ma ◽  
Liang Zhou

IntroductionThe long non-coding RNA HULC has been shown to be involved in the development of several human cancers. The present study was undertaken to investigate the regulatory role of lncRNA-HULC in growth and metastasis of human glioma.Material and methodsThe gene expression of lncRNA-HULC was estimated from the clinical glioma tissues and cell lines using RT-PCR. The proliferation of transfected cancer cells was determined with the help of cell counting kit-8 (CCK8). DAPI staining and dual annexin V-FITC/PI staining procedures were used for inferring the apoptosis of transfected cancer cells. Scratch-heal and transwell chamber assays were employed for the determination of migration and invasion of transfected cells. The expression of proteins of interest was studied by western blotting technique.ResultsThe results showed that lncRNA-HULC exhibits significantly (p < 0.05) higher expression in glioma tissues and cancer cells. The knockdown of lncRNA-HULC led to a marked decline in the proliferation of glioma cells through apoptotic induction which was accompanied by upregulation of Bax and downregulation of Bcl-2. Moreover, knockdown of lncRNA-HULC significantly (p < 0.05) suppressed the migration and invasion of cancer cells in vitro. The western blot analysis showed that lncRNA-HULC exerted its effects via modulation of the PI3K/AKT signaling pathway.ConclusionsThe study revealed the possibility of targeting the PI3K/AKT signaling pathway in glioma through transcriptional knockdown of lncRNA-HULC, which might be utilized for therapeutic purposes against human glioma.


2017 ◽  
Vol 16 (3) ◽  
pp. 2946-2952 ◽  
Author(s):  
Binbin Ma ◽  
Zebin Gao ◽  
Jiacheng Lou ◽  
Hongqiang Zhang ◽  
Zhongbo Yuan ◽  
...  

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 921-931
Author(s):  
Juan Zhao ◽  
Xue-Bin Zeng ◽  
Hong-Yan Zhang ◽  
Jie-Wei Xiang ◽  
Yu-Song Liu

AbstractLong non-coding RNA forkhead box D2 adjacent opposite strand RNA 1 (FOXD2-AS1) has emerged as a potential oncogene in several tumors. However, its biological function and potential regulatory mechanism in glioma have not been fully investigated to date. In the present study, RT-qPCR was conducted to detect the levels of FOXD2-AS1 and microRNA (miR)-506-5p, and western blot assays were performed to measure the expression of CDK2, cyclinE1, P21, matrix metalloproteinase (MMP)7, MMP9, N-cadherin, E-cadherin and vimentin in glioma cells. A luciferase reporter assay was performed to verify the direct targeting of miR-506-5p by FOXD2-AS1. Subsequently, cell viability was analyzed using the CCK-8 assay. Cell migration and invasion were analyzed using Transwell and wound healing assays, respectively. The results demonstrated that FOXD2-AS1 was significantly overexpressed in glioma cells, particularly in U251 cells. Knockdown of FOXD2-AS1 in glioma cells significantly inhibited cell proliferation, migration, invasion and epithelial–mesenchymal transition (EMT) and regulated the expression of CDK2, cyclinE1, P21, MMP7 and MMP9. Next, a possible mechanism for these results was explored, and it was observed that FOXD2-AS1 binds to and negatively regulates miR-506-5p, which is known to be a tumor-suppressor gene in certain human cancer types. Furthermore, overexpression of miR-506-5p significantly inhibited cell proliferation, migration, invasion and EMT, and these effects could be reversed by transfecting FOXD2-AS1 into the cells. In conclusion, our data suggested that FOXD2-AS1 contributed to glioma proliferation, metastasis and EMT via competitively binding to miR-506-5p. FOXD2-AS1 may be a promising target for therapy in patients with glioma.


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