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LncRNA NFIA-AS2 promotes glioma progression through modulating the miR-655-3p/ZFX axis

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Abstract

Long non-coding RNAs (lncRNAs) are closely associated with tumorigenesis of various malignancies, including glioma. However, the roles of most lncRNAs in glioma remain undiscovered. The present study for the first time explored the roles of NFIA-AS2 in glioma. Based on informatic analyses by online database, lncRNA NFIA-AS2 in glioma tissues was overexpressed and further confirmed in glioma tissues and cells by quantitative real-time PCR (qRT-PCR). High expression of NFIA-AS2 was closely correlated with poor prognosis and might be an independent prognostic factor for PFS and OS. Functionally, silenced NFIA-AS2 could remarkably hinder glioma cell proliferation, migration and invasion, and cause the apoptosis. Mechanistic investigation disclosed that NFIA-AS2 interacted with miR-655-3p and inversely connected with miR-655-3p in glioma. Additionally, miR-655-3p was proved to regulate the expression of ZFX. Final rescue assay demonstrated that ZFX overexpression or miR-655-3p downregulation could neutralize the suppressive effects of NFIA-AS2 knockdown on glioma progression. In conclusion, this study firstly reported that NFIA-AS2 could promote the progression of glioma by targeting the miR-665-3p/ZFX axis, which highlighted that NFIA-AS2 could be a novel biomarker and therapeutic target for glioma patients.

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Contributions

L-QT designed the experiments, analyzed data and wrote the manuscript. JX and L-HZ completed the experiments, collected the data and revised the manuscript. X-YZ collected the data and analyzed data. All authors approved the submission and were responsible for the authenticity of this manuscript.

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Correspondence to Li-Qiang Tian.

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This research was approved by the Ethics Committee of Linyi People’s Hospital.

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Xin, J., Zhao, YH., Zhang, XY. et al. LncRNA NFIA-AS2 promotes glioma progression through modulating the miR-655-3p/ZFX axis. Human Cell 33, 1273–1280 (2020). https://doi.org/10.1007/s13577-020-00408-9

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  • DOI: https://doi.org/10.1007/s13577-020-00408-9

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