Long noncoding RNA NEAT1 regulates glioma cells proliferation and apoptosis by competitively binding with miR-324-5p and upregulating KCTD20 expression

Abstract

Background Recent studies have pointed out that long non-coding RNAs (lncRNAs) play a key role in tumorigenesis, including glioma. Nuclear paraspeckle assembly transcript 1 (NEAT1), a lncRNA, has been reported to be participated in the development and progression of many types of tumors and promotes cancer cell proliferation, migration, invasion, and drug resistance. The exact role and regulatory mechanism of NEAT1 in gliomas still need to be further explored. Methods NEAT1 expression was detected in paired glioma tissues and adjacent normal tissues, as well as in glioma cell lines by quantitative real-time PCR (qRT-PCR). Cell viability and apoptosis were measured using flow cytometry, colony formation assays and TdT-mediated dUTP nick-end labeling (TUNEL) assay. The mechanism of competing endogenous RNA (ceRNA) between NEAT1 and miR-324-5p was determined using bioinformatics analysis, RIP and luciferase reporter assay. Results Here we demonstrated that lncRNA NEAT1 was upregulated and significantly associated with poor prognosis in glioma tissues. Through gain- and loss-of NEAT1 expression, we found that knockdown of NEAT1 inhibited the abilities of cell proliferation and induced G0/G1 arrest and apoptosis in vitro, suppressed tumorigenesis in vivo via sponging miR-324-5p and then upregulated KCTD20 expression. In addition, NEAT1 reversed the effects of miR-324-5p on the proliferation and apoptosis of glioma cells, and involved the inhibition of potassium channel tetramerization protein domain containing 20 (KCTD20) expression. Conclusion Collectively, our findings demonstrate that NEAT1 epigenetically up-regulates KCTD20 expression through competitively binding miR-324-5p, and also provides a potential therapeutic target for human glioma.