Research Papers:

This article has been retracted. Retraction in: Oncotarget. 2024; 15:255-255.

Knockdown of NEAT1 restrained the malignant progression of glioma stem cells by activating microRNA let-7e

Wei Gong, Jian Zheng, Xiaobai Liu, Jun Ma, Yunhui Liu and Yixue Xue _

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Oncotarget. 2016; 7:62208-62223. https://doi.org/10.18632/oncotarget.11403

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Wei Gong1,2, Jian Zheng3,4, Xiaobai Liu3,4, Jun Ma1,2, Yunhui Liu3,4, Yixue Xue1,2

1Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang 110122, People’s Republic of China

2Institute of Pathology and Pathophysiology, China Medical University, Shenyang 110122, People’s Republic of China

3Department of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, People’s Republic of China

4Liaoning Research Center for Translational Medicine in Nervous System Disease, Shenyang 110004, People’s Republic of China

Correspondence to:

Yixue Xue, email: [email protected]

Keywords: lncRNAs, NEAT1, glioma stem cells, let-7e, NRAS

Received: March 18, 2016    Accepted: August 09, 2016    Published: August 19, 2016


Nuclear paraspeckle assembly transcript 1 (NEAT1), a long non-coding RNA, promotes oncogenesis in various tumors, including human gliomas. Herein, we studied the expression and function of NEAT1 in glioma stem cells (GSCs). Quantitative real-time PCR demonstrated that NEAT1 was upregulated in GSCs. NEAT1 knockdown inhibited GSC cell proliferation, migration and invasion and promoted GSC apoptosis. A potential binding region between NEAT1 and microRNA let-7e was confirmed by dual-luciferase assays. Upregulation of NEAT1 reduced the expression of let-7e, and there was reciprocal repression between NEAT1 and let-7e in an Argonaute 2-dependent manner. Let-7e expression was lower expression in glioblastoma tissues and GSCs than in normal brain tissues and cells. Restoration of let-7e suppressed tumor function by inhibiting proliferation, migration and invasion while promoting apoptosis in GSCs. NEAT1 knockdown and let-7e overexpression both reduced NRAS protein expression. NRAS was identified as a direct target of let-7e and promoted oncogenesis in GSCs. As NEAT1 promoted oncogenesis by downregulating let-7e expression, both of these genes could be considered for application in glioma therapy.

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