4.4 Article

Long non-coding RNA NBAT1 inhibits the progression of glioma through the miR-21/SOX7 axis

Journal

ONCOLOGY LETTERS
Volume 20, Issue 3, Pages 3024-3034

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2020.11847

Keywords

glioma; long non-coding RNA NBAT1; proliferation; migration; invasion

Categories

Funding

  1. Outstanding Talent Cultivation Foundation of Liaoning Province [2015020349]
  2. President Foundation of Jinzhou Medical University [XZJJ20130206]
  3. Natural Science Foundation of Liaoning Province [2019-ZD-0824]

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Glioma is one of the most prevalent types of malignancy in the central nervous system worldwide, and the prognosis of patients with late stage glioma remains poor. Thus, the development of promising therapeutic strategies against glioma is essential. Long non-coding RNAs (lncRNAs) are functional RNA molecules involved in the initiation and progression of tumors, including glioma. Investigation on the regulatory roles of lncRNAs may facilitate the development of effective treatments. lncRNA NBAT1 is associated with the growth and metastasis of cancer; however, its underlying molecular mechanisms remain unknown. Thus, the present study aimed to investigate the effects of NBAT1 in glioma. The expression levels of NBAT1, microRNA (miRNA/miR)-21 and SOX7 in patients with glioma, and healthy donors using reverse transcription-quantitative PCR analysis. Human glioma cells (A172 and AM138) and normal astrocytes were used to establish the NBAT1-knockdown and overexpression models. Cell Counting Kit-8 and Transwell assays were performed to determine whether NBAT1 exerted effects on cell proliferation, migration and invasion. The results demonstrated that NBAT1 expression decreased in glioma tissues compared to normal samples. Additionally, downregulation of NBAT1 was detected in human glioma cells compared with normal astrocytes. Overexpression of NBAT1 inhibited glioma cell proliferation, migration and invasion. In addition, miR-21 was identified as a potential target of NBAT1, and the effects of miR-21-induced cell proliferation and metastasis were reversed following overexpression of NBAT1. Furthermore, SOX7 was predicted as the potential target of miR-21, and its expression was upregulated in glioma cells by overexpression of NBAT1 compared with the vehicle only control. Taken together, the results of the present study provide novel insight into the functions of NBAT1 in glioma, suggesting that the NBAT1/miR-21/SOX7 axis may act as a potential therapeutic target for the treatment of patients with glioma.

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