OBJECTIVE: The specific roles of long noncoding RNAs (lncRNAs) have been found in human cancers, including retinoblastoma (RB). However, the function of lncRNA-NORAD has not been reported in RB. Therefore, the regulatory mechanism of lncRNA-NORAD was investigated in the development of RB.
PATIENTS AND METHODS: The experimental tissues were collected from 24 RB patients and 6 patients with ruptured globes. The average age of all patients was 2.78 years (range, 2 months to 11 years). The mRNA and protein expression was measured by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) and Western blot analysis. The functional mechanism of NORAD was assessed by Cell Counting Kit-8 (CCK-8), transwell, and Dual-Luciferase reporter assays.
RESULTS: Upregulation of NORAD and downregulation of miR-136-5p were found in RB. Functionally, knockdown of NORAD and miR-136-5p overexpression restrained RB cell viability, invasion, and migration. In addition, NORAD acts as a ceRNA of miR-136-5p in RB. MiR-136-5p was found to directly target PBX3. Furthermore, knockdown of PBX3 inhibited the progression of RB. More importantly, the NORAD/miR-136-5p axis is involved in RB progression by mediating PBX3.
CONCLUSIONS: LncRNA NORAD, serving as a ceRNA of miR-136-5p, accelerates RB progression by upregulation of PBX3.
This article has been withdrawn. The Publisher apologizes for any inconvenience this may cause.Free PDF Download
To cite this article
X.-L. Yang, Y.-J. Hao, B. Wang, X.-L. Gu, X.-X. Wang, J.-F. Sun
Long noncoding RNA NORAD promotes the progression of retinoblastoma by sponging miR-136-5p/PBX3 axis
Eur Rev Med Pharmacol Sci
Vol. 24 - N. 3