Department of Urology, Tengzhou Central People's Hospital, Tengzhou, China.
Eur Rev Med Pharmacol Sci. 2020 Oct;24(20):10426-10432. doi: 10.26355/eurrev_202010_23394.
The purpose of this study was to clarify the potential role of long non-coding RNA (lncRNA) NORAD in the development of renal cancer.
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.
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.
LncRNA NORAD stimulates proliferative and migratory potentials in renal cancer by sponging miR-144-3p to upregulate MYCN.
本研究旨在阐明长链非编码 RNA（lncRNA）NORAD 在肾癌发展中的潜在作用。
检测肾癌组织和细胞系中 NORAD、miR-144-3p 和 MYCN 的表达水平。过表达 NORAD 后，通过细胞计数试剂盒-8（CCK-8）和 Transwell 检测分别评估 ACHN 和 A498 细胞的增殖和迁移变化。随后，通过荧光素酶测定来确定 NORAD/miR-144-3p/MYCN 轴的相互作用。此外，通过挽救实验最终证明了其在影响肾癌细胞表型变化中的生物学功能。
结果表明，NORAD 和 MYCN 在肾癌组织中上调，而 miR-144-3p 下调。NORAD 的过表达刺激了 ACHN 和 A498 细胞的增殖和迁移潜能，而 miR-144-3p 的共过表达部分消除了这些潜能。此外，还发现 NORAD/miR-144-3p/MYCN 轴负责刺激肾癌的恶性发展。
lncRNA NORAD 通过海绵吸附 miR-144-3p 来上调 MYCN，从而刺激肾癌的增殖和迁移潜能。
