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Long Intergenic Non-Protein Coding RNA 1094 Promotes Initiation and Progression of Glioblastoma by Promoting microRNA-577-Regulated Stabilization of Brain-Derived Neurotrophic Factor

Authors Dong X, Fu X, Yu M, Li Z

Received 30 March 2020

Accepted for publication 9 June 2020

Published 9 July 2020 Volume 2020:12 Pages 5619—5631


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Ahmet Emre Eskazan

Xiaoyan Dong,1 Xiuxin Fu,1 Miao Yu,1 Zengfen Li2

1Department of Hepatobiliary Surgery, Weifang People’s Hospital, Weifang, Shandong 261000, People’s Republic of China; 2Brain Hospital, Weifang People’s Hospital, Weifang, Shandong 261000, People’s Republic of China

Correspondence: Zengfen Li
Brain Hospital, Weifang People’s Hospital, 151 Guangwen Road, Weifang, Shandong 261000, People’s Republic of China

Purpose: The long intergenic non-protein coding RNA 1094 (LINC01094) plays a vital role in the oncogenicity of clear cell renal cell carcinoma. However, its expression profile and detailed roles in glioblastoma (GBM) remain unknown. In this study, we mainly investigated the expression and roles of LINC01094 in GBM and focused on the mechanism by which LINC01094 regulates the malignant characteristics of GBM.
Patients and Methods: LINC01094 expression in GBM was determined with quantitative reverse transcription polymerase chain reaction. The proliferation, apoptosis, migration, invasion in vitro, and tumor growth in vivo of GBM cells were evaluated using Cell Counting Kit-8 assay, flow cytometry analysis, migration assay, invasion assay, and tumor xenograft models, respectively.
Results: LINC01094 was overexpressed in GBM tissues and cell lines. Moreover, increased LINC01094 expression was associated with adverse clinicopathological parameters in patients with GBM. Loss of LINC01094 inhibited GBM cell proliferation, migration, and invasion; promoted cell apoptosis; and suppressed tumor growth in vivo. Mechanically, LINC01094 functioned as a molecular sponge for microRNA-577 (miR-577) and consequently enhanced the expression of brain-derived neurotrophic factor (BDNF) in GBM cells. Both miR-577 inhibition and BDNF expression enhancement reversed LINC01094 deficiency-mediated inhibition of malignant processes in GBM cells.
Conclusion: Our results verified the involvement of the LINC01094/miR-577/BDNF pathway in GBM cells and its enhancing effects on the aggressive behaviors of GBM cells in vitro and in vivo. This pathway may be a novel and promising focus for the future development of targeted therapies for GBM.

Keywords: long intergenic non-protein coding RNA, glioblastoma, microRNA, brain-derived neurotrophic factor

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