W Zhao1, L Wang, F Xu. 1. Department of Urology, Tengzhou Central People's Hospital, Tengzhou, China. jwjc@mail.jnmc.edu.cn.
Abstract
OBJECTIVE: The purpose of this study was to clarify the potential role of long non-coding RNA (lncRNA) NORAD in the development of renal cancer. PATIENTS AND METHODS: Expression levels of NORAD, miR-144-3p, and MYCN in renal cancer tissues and cell lines were detected. After overexpression of NORAD, proliferative and migratory changes in ACHN and A498 cells were evaluated by Cell Counting Kit-8 (CCK-8) and transwell assay, respectively. Thereafter, Luciferase assay was conducted to determine the interaction in the NORAD/miR-144-3p/MYCN axis. Besides, its biological function in influencing phenotype changes of renal cancer cells was finally demonstrated by rescue experiments. RESULTS: The results manifested that NORAD and MYCN were upregulated, while miR-144-3p was downregulated in renal cancer tissues. Overexpression of NORAD stimulated proliferative and migratory potentials in ACHN and A498 cells, which were partially abolished by co-overexpression of miR-144-3p. Moreover, NORAD/miR-144-3p/MYCN axis was found to be responsible for stimulating the malignant development of renal cancer. CONCLUSIONS: LncRNA NORAD stimulates proliferative and migratory potentials in renal cancer by sponging miR-144-3p to upregulate MYCN.
OBJECTIVE: The purpose of this study was to clarify the potential role of long non-coding RNA (lncRNA) NORAD in the development of renal cancer. PATIENTS AND METHODS: Expression levels of NORAD, miR-144-3p, and MYCN in renal cancer tissues and cell lines were detected. After overexpression of NORAD, proliferative and migratory changes in ACHN and A498 cells were evaluated by Cell Counting Kit-8 (CCK-8) and transwell assay, respectively. Thereafter, Luciferase assay was conducted to determine the interaction in the NORAD/miR-144-3p/MYCN axis. Besides, its biological function in influencing phenotype changes of renal cancer cells was finally demonstrated by rescue experiments. RESULTS: The results manifested that NORAD and MYCN were upregulated, while miR-144-3p was downregulated in renal cancer tissues. Overexpression of NORAD stimulated proliferative and migratory potentials in ACHN and A498 cells, which were partially abolished by co-overexpression of miR-144-3p. Moreover, NORAD/miR-144-3p/MYCN axis was found to be responsible for stimulating the malignant development of renal cancer. CONCLUSIONS: LncRNA NORAD stimulates proliferative and migratory potentials in renal cancer by sponging miR-144-3p to upregulate MYCN.