Retinoblastoma (RB) is an intraocular malignancy that mainly affects young children. Previous reports have demonstrated that mutations or the inactivation of the RB1 gene were the main cause of RB; however, disruption of the intracellular signaling pathways following deficiency of RB1 requires further investigation. Based on the Gene Expression Omnibus data and bioinformatics prediction, the present study aimed to investigate the microRNA (miR)‑338‑3p/neuro‑oncological ventral antigen 1 (NOVA1) axis in RB. Subsequently, overexpression and knockdown of miR‑338‑3p and NOVA1, respectively, were performed to study the role of miR‑338‑3p/NOVA1 in the progression of the RB cells. The results demonstrated that overexpression of miR‑338‑3p significantly inhibited cell proliferation, migration and invasion, and promoted apoptosis of the RB cells. Moreover, knockdown of NOVA1 showed similar results. A dual‑luciferase reporter assay and rescue experiments further confirmed the direct binding between miR‑338‑3p and NOVA1. Taken together, the results indicated that miR‑338‑3p acted as tumor suppressor by targeting the oncogene of NOVA1 in RB, which may serve as potential therapeutic targets in RB.
Keywords: microRNA‑338‑3p; neuro‑oncological ventral antigen 1; retinoblastoma.