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LncRNA-NNT-AS1 contributes to the progression of glioma by miR-582-5p/EZH2 axis

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Abstract

Increasing studies have shown that long non-coding RNAs (lncRNAs) had crucial regulatory roles in many diseases. Nevertheless, the biological relevance and mechanisms of the NNT-AS1 in gliom remain poorly understood. In the present study, NNT-AS1 expression was up-regulated in the glioma cell lines. Functional assays demonstrated that depletion of NNT-AS1 could notably suppress the proliferation, migration, invasion and EMT of U87MG and A172 cells. In addition, miR-582-5p was predicted to be a target of NNT-AS1 and EZH2 was predicted to be a target of miR-582-5p by bioinformatics software, which was further confirmed by luciferase reporter assay. Additionally, results of recue assays proofed that NNT-AS1/miR-582-5p/EZH2 axis aggravated the malignant behaviors of glioma. Ultimately, our findings revealed that NNT-AS1 contributes to progression via targeting miR-582-5p/EZH2 axis, revealing NNT-AS1 as a latent effective target for the diagnosis and treatment of glioma patients.

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Data availability

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

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Acknowledgements

We deeply appreciate the supports by all participants.

Funding

This study was supported by National Youth Natural Science Foundation (Grant No. 81500914) and Chinese Postdoctoral Science Foundation (Grant No. 2018M632381).

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Authors and Affiliations

  1. The Department of Physiology, Xuzhou Medical University, 209th Tongshan Road, Xuzhou, 221004, Jiangsu Province, People’s Republic of China

    Tonglin Pan & Min Xue

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  1. Tonglin Pan
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  2. Min Xue
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Contributions

MX conceived and designed the study and drafted the manuscript. TP collected and analyzed the data. All authors read and approved the final manuscript.

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Correspondence to Min Xue.

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Pan, T., Xue, M. LncRNA-NNT-AS1 contributes to the progression of glioma by miR-582-5p/EZH2 axis. Cytotechnology 73, 473–482 (2021). https://doi.org/10.1007/s10616-021-00471-6

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  • DOI: https://doi.org/10.1007/s10616-021-00471-6

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