Affordable Access

deepdyve-link
Publisher Website

lncRNA CCAT1 Promotes Glioma Tumorigenesis by Sponging miR-181b.

Authors
  • Cui, Bingzhou1
  • Li, Baoshan2
  • Liu, Qi3
  • Cui, Youqiang4
  • 1 Department of Neurosurgery, The People's Hospital of Zhengzhou, Zhengzhou, 450002 Henan, China. , (China)
  • 2 Department of Neurosurgery, The Third People's Hospital of Qingdao, Qingdao, 266041, Shandong, China. , (China)
  • 3 Department of Neurosurgery, Brain Hospital, People's Hospital of Weifang, Weifang, 261021, Shandong, China. , (China)
  • 4 Department of Neurosurgery, Qianfoshan Hospital Affiliated to Shandong University, Jinan, 250014, Shandong, China. , (China)
Type
Published Article
Journal
Journal of Cellular Biochemistry
Publisher
Wiley (John Wiley & Sons)
Publication Date
Dec 01, 2017
Volume
118
Issue
12
Pages
4548–4557
Identifiers
DOI: 10.1002/jcb.26116
PMID: 28475287
Source
Medline
Keywords
License
Unknown

Abstract

Colon cancer-associated transcript 1 (CCAT1), a long non-coding RNA (lncRNA), is upregulated and has a vital role in the pathogenesis of numerous cancers. Recently, its high expression was found in glioma tissues. miR-181b is downregulated in glioma and acts as a tumor suppressor. However, the exact mechanism of CCAT1 action in the regulation of glioma development remains unknown. CCAT1 and miR-181b expression was firstly examined in glioma tissue samples by real-time PCR. An RNA interference approach was used to downregulate CCAT1 expression and we analyzed the underlying mechanism of CCAT1 by using bioinformatics analysis, CCK-8 assay, Transwell assay, flow cytometry, luciferase assay, RNA immunoprecipitation, real-time PCR, Western blot, and xenograft models. CCAT1 expression was significantly increased, while miR-181b decreased, in glioma tissues. Interestingly, miR-181b expression was negatively correlated with the CCAT1 level in glioma samples. Knockdown of CCAT1 notably suppressed proliferation, migration and the epithelial-mesenchymal transition (EMT) process, and promoted the apoptosis of U87 and LN229 glioma cells, which could be enhanced by transfection with miR-181b mimic while it was abolished by anti-miR-181b. Additionally, we found that CCAT1 may act as a competing endogenous RNA (ceRNA) for miR-181b, regulating the de-repression of FGFR3 and PDGFRα. In conclusion, CCAT1 promotes glioma tumorigenesis by sponging miR-181b, leading to the de-repression of its endogenous targets FGFR3 and PDGFRα, which provides a potential therapeutic target for glioma treatment. J. Cell. Biochem. 118: 4548-4557, 2017. © 2017 Wiley Periodicals, Inc.

Report this publication

Statistics

Seen <100 times