Suppression of long non-coding RNA UCA1 inhibits proliferation and invasion and induces apoptosis in human lung cancer cells

T. Jun, F.-S. Zheng, K.-M. Ren, H.-Y. Zhang, J.-G. Zhao, J.-Z. Zhao

Department of The First Thoracic Surgery, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, People’s Republic of China. zhaojz@sj-hospital.org

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• Oncology

OBJECTIVE: Lung cancer is one of the deadliest cancers responsible for significant mortality and morbidity across the globe. The unavailability of efficient treatments, lack of reliable biomarkers and potent therapeutic targets, limit the treatment of lung cancer. In this study, we explored the potential of long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) as the therapeutic target for lung cancer.

MATERIALS AND METHODS: The expression analysis was carried out by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell viability was monitored by cell counting kit 8 (CCK-8) assay. The 4′,6-diamidino-2-phenylindole (DAPI), annexin-V/Propidium iodide staining and comet assays were used to detect apoptosis. Boyden chamber and wound heal assays were used for cell to asses cell invasion and migration respectively. Protein expression was determined by immunoblotting.

RESULTS: The expression of lncRNA UCA1 was determined by qRT-PCR in six different types of lung cancer cell lines. It was observed that lncRNA UCA1 was significantly (p < 0.05) upregulated in all the lung cancer cell lines. To investigate the role of lncRNA UCA1 in lung cancer, its expression was suppressed by transfection of the lung cancer NCI-H23 cells by si-UCA1. The results showed that suppression of lncRNA UCA1 significantly (p < 0.05) reduced the viability of NCI-H23 cancer cells via induction of the apoptosis. Furthermore, the lncRNA UCA1 suppression (p < 0.05) significantly inhibited the migration and invasion of the NCI-H23 lung cancer at least in part via inhibition of mitogen-activated protein kinase 1 (MAPK1). Additionally, the suppression of MAPK1 exhibited similar effects on the proliferation, migration, and invasion of the NCI-H23 cells as that of UCA1 silencing. Finally, the co-suppression of lncRNA UCA1 and MAPK1 exhibited synergistic effects on cell proliferation, migration, and invasion.

CONCLUSIONS: We demonstrated that lncRNA UCA1 could be an important therapeutic target for curbing lung cancer.

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