LncRNA NEAT1/miR-1224/KLF3 contributes to cell proliferation, apoptosis and invasion in lung cancer

The aim of this study was to detect the relationship between long-chain non-coding RNA (lncRNA) NEAT1 and microRNA-1224 (miR-1224) in lung cancer and to explore its underlying mechanism. The expression levels of lncRNA NEAT1 and miR-1224 in lung cancer tissues and cells were detected by quantitative...

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Published inEuropean review for medical and pharmacological sciences Vol. 23; no. 19; p. 8403
Main Authors Yu, P-F, Wang, Y, Lv, W, Kou, D, Hu, H-L, Guo, S-S, Zhao, Y-J
Format Journal Article
LanguageEnglish
Published Italy 01.10.2019
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Summary:The aim of this study was to detect the relationship between long-chain non-coding RNA (lncRNA) NEAT1 and microRNA-1224 (miR-1224) in lung cancer and to explore its underlying mechanism. The expression levels of lncRNA NEAT1 and miR-1224 in lung cancer tissues and cells were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The interaction between lncRNA NEAT1 with miR-1224, miR-1224, and KLF3 was detected by Dual-Luciferase Reporter Gene Assay. MTT 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and flow cytometry were used to detect the changes in the proliferative and apoptosis abilities of lung cancer cells after silencing lncRNA NEAT1 or up-regulating miR-1224, respectively. Compared with adjacent normal tissues, lncRNA NEAT1 was significantly up-regulated, while miR-1224 was significantly down-regulated in lung cancer tissues. LncRNA NEAT1 could specifically bind to the 3'UTR of miR-1224 and regulate its expression. The inhibition of lncRNA NEAT1 remarkably reduced the proliferation and enhanced the apoptosis of lung cancer cells. However, the upregulation of the expression of miR-1224 level could significantly inhibit proliferation and promote the apoptosis rate of lung cancer cells. Furthermore, miR-1224 could downregulate KLF3 expression by directly binding to its 3'UTR. LncRNA NEAT1 can sponge the expression of miR-1224, thereby affecting the proliferation and apoptosis of lung cancer.
ISSN:2284-0729
DOI:10.26355/eurrev_201910_19151