4.7 Article

Long noncoding RNA nuclear enriched abundant transcript 1 impacts cell proliferation, invasion, and migration of glioma through regulating miR-139-5p/CDK6

Journal

JOURNAL OF CELLULAR PHYSIOLOGY
Volume 234, Issue 5, Pages 5972-5987

Publisher

WILEY
DOI: 10.1002/jcp.27093

Keywords

CDK6; glioma; invasion; long noncoding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1); migration; miR-139-5p; nude mouse model; proliferation

Funding

  1. National Natural Science Foundation of China [81271225, 81400902, 31201039, 30950031, 81571055, 81171012]
  2. Major Fundamental Resarch Program of the Natural Science Foundation of the Jiangsu Higher Education Institutions of China [13KJA180001]
  3. Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
  4. 2016 333 Project Award of Jiangsu Province
  5. 2013 Qinglan Project of the Young and Middle-aged Academic Leader of Jiangsu College and University
  6. Cultivate National Science Fund for Distinguished Young Scholars of Jiangsu Normal University

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Aims: We aimed to explore the impact of long noncoding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) on cell proliferation, invasion, and migration of glioma. Methods: Differentially expressed genes were screened out from Gene Expression Omnibus data set based on the microarray analysis. The expression levels of lncRNA NEAT1, miR-139-5p, and CDK6 in glioma cells and tissues were examined by quantitative reverse transcription polymerase chain reaction, and the protein level of CDK6 in glioma cells was determined by western blot and immunohistochemistry. Glioma cell viability, cell cycle, and apoptosis were detected by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) and flow cytometry, respectively, whereas cell invasion and migration were analyzed by transwell assay. The target relationships among NEAT1, miR-139-5p, and CDK6 were confirmed by dual-luciferase reporter gene assay. The effects of lncRNA NEAT1 on tumor growth were further testified through glioma xenografts in nude mice. Results: LncRNA NEAT1 and CDK6 were highly expressed in glioma tissues and cells, whereas miR-139-5p was lowly expressed. There were target relationships and correlations on expressions between miR-139-5p and NEAT1/ CDK6. NEAT1 and CDK6 could promote cell proliferation and metastasis of glioma cells and impeded cell apoptosis, whereas miR-139-5p exerted suppressive effects on the biological functions of glioma cells. NEAT1 regulated CDK6 to affect glioma growth through sponging miR-139-5p. Conclusions: LncRNA NEAT1 promotes cell proliferation, invasion, and migration of glioma through regulating miR-139-5p/CDK6 pathway.

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