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

P.-F. Yu, Y. Wang, W. Lv, D. Kou, H.-L. Hu, S.-S. Guo, Y.-J. Zhao

Department of Respiratory Medicine, Yantai Yuhuangding Hospital, Yantai, China. zhaoyongjuan1987@163.com

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• Oncology

OBJECTIVE: 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.
MATERIALS AND METHODS: 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.
RESULTS: 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.
CONCLUSIONS: LncRNA NEAT1 can sponge the expression of miR-1224, thereby affecting the proliferation and apoptosis of lung cancer.

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