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Long-Noncoding RNA FGD5-AS1 Enhances the Viability, Migration, and Invasion of Glioblastoma Cells by Regulating the miR-103a-3p/TPD52 Axis

Authors Su D, Ji Z, Xue P, Guo S, Jia Q, Sun H

Received 11 March 2020

Accepted for publication 8 July 2020

Published 27 July 2020 Volume 2020:12 Pages 6317—6329


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Eileen O'Reilly

Daoqing Su, Zhengang Ji, Pengfei Xue, Shengfu Guo, Qingbin Jia, Hanyu Sun

Department of Neurosurgery, Liaocheng People’s Hospital and Liaocheng Brain Hospital, Liaocheng Hospital Affiliated to Shandong First Medical University, Liaocheng City, Shandong Province, People’s Republic of China

Correspondence: Hanyu Sun Tel +86-18365751192

Purpose: This study was designed to explore the functional role of FYVE, RhoGEF, and PH domain containing 5 antisense RNA 1 (FGD5-AS1) and the underlying regulatory mechanism in the progression of glioblastoma (GBM).
Materials and Methods: FGD5-AS1 expression was analyzed in The Cancer Genome Atlas (TCGA), and then detected in GBM tissues and cells by quantitative reverse-transcription polymerase chain reaction. Viability, migration, and invasion of GBM cells were assessed using the MTT, wound healing, and transwell assays, respectively. StarBase/TargetScan analysis and dual-luciferase reporter gene (DLR) assay were performed to investigate the relationship between FGD5-AS1/tumor protein D52 (TPD52) and miR-103a-3p. A xenograft tumor model was established to evaluate the role of FGD5-AS1 in GBM tumorigenesis in vivo.
Results: FGD5-AS1 was overexpressed in GBM tissues and cells, and silencing of FGD5-AS1 expression resulted in the inhibition of the viability, migration, and invasion of GBM cells. miR-130-3p was a target of FGD5-AS1, and its expression was negatively regulated by FGD5-AS1. Silencing miR-103a-3p expression resulted in the abrogation of the inhibitory effects of si-FGD5-AS1 on the viability, migration, and invasion of GBM cells. TPD52 was a target of miR-103a-3p and suppressed the antitumor effects of FGD5-AS1 silencing on GBM cells. In addition, FGD5-AS1 silencing inhibited the growth of xenograft tumors in vivo by modulating the miR-103a-3p/TPD52 axis.
Conclusion: Silencing of FGD5-AS1 inhibited the viability, migration, and invasion of GBM cells by regulating the miR-103a-3p/TPD52 axis.

Keywords: glioblastoma, FGD5-AS1, viability, migration, invasion, miR-103a-3p, TPD52

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