OncoTargets and Therapy (Sep 2019)

lncRNA LINC01494 Promotes Proliferation, Migration And Invasion In Glioma Through miR-122-5p/CCNG1 Axis

  • Li C,
  • Hu G,
  • Wei B,
  • Wang L,
  • Liu N

Journal volume & issue
Vol. Volume 12
pp. 7655 – 7662

Abstract

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Chang Li,1,* Guozhang Hu,2,* Bo Wei,3 Le Wang,4 Naijie Liu3 1Department of VIP Unit, China-Japan Union Hospital of Jilin University, Changchun 130031, People’s Republic of China; 2Department of First-aid Medicine, China-Japan Union Hospital of Jilin University, Changchun 130031, People’s Republic of China; 3Department of Neurosurgery, China-Japan Union Hospital of Jilin University, Changchun 130031, People’s Republic of China; 4Department of Ophthalmology, The First Hospital of Jilin University, Changchun 130021, People’s Republic of China*These authors contributed equally to this workCorrespondence: Naijie LiuDepartment of Neurosurgery, China-Japan Union Hospital of Jilin University, 126 Xiantai Street, Changchun 130031, People’s Republic of ChinaTel +86 431186 4310 7700Email [email protected]: Long noncoding RNAs (lncRNAs) are recognized as key effectors in tumor, including glioma. LINC01494 is an uncharacterized novel lncRNA. In this research, we aimed to investigate the function of LINC01494 in glioma.Methods: Gene relative expression was analyzed by qRT-PCR method. CCK8, colony formation and Transwell assay was used to determine cell proliferation, migration and invasion. Bioinformatics analyses were used to predict the target of LINC01494 and miR-122-5p. Luciferase reporter assay was utilized to validate the interactions between LINC01494 and miR-122-5p or CCNG1 and miR-122-5p.Results: LINC01494 was identified as a significantly upregulated lncRNA in glioma through bioinformatics analysis. Furthermore, LINC01494 upregulation indicated poor prognosis. Meanwhile, in vitro investigation indicated that silencing LINC01494 with siRNAs obviously inhibited the proliferation, cell cycle, migration and invasion of glioma cells. Besides, it is found that LINC01494 expression was negatively correlated with miR-122-5p. We demonstrated that LINC01494 inhibited miR-122-5p to upregulate CCNG1 expression through direct interaction. Rescue assay further demonstrated that LINC01494/miR-122-5p/CCNG1 signaling cascade plays a critical role in regulating glioma cell proliferation, migration and invasion.Conclusion: Taken together, our findings demonstrated the essential function and molecular mechanism of LINC01494 in glioma progression.Keywords: LINC01494, miR-122-5p, CCNG1, glioma, proliferation

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