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Updated: Nov 11, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
Roles of the microRNA‑338‑3p/NOVA1 axis in retinoblastoma
Shoubin Sun1, Runze Wang2, Sisi Yi2
1Department of Ophthalmology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Abstract:
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.
Insights
MicroRNA-338-3p acts as a tumor suppressor in retinoblastoma (RB) by targeting NOVA1. This finding reveals a new therapeutic strategy for treating this childhood eye cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Retinoblastoma (RB) is a primary intraocular cancer in children.
- RB1 gene mutations are primary causes, but downstream signaling disruptions need study.
Purpose of the Study:
- Investigate the microRNA (miR)‑338‑3p/neuro‑oncological ventral antigen 1 (NOVA1) axis in RB.
- Determine the role of miR‑338‑3p/NOVA1 in RB cell progression.
Main Methods:
- Bioinformatics analysis of Gene Expression Omnibus data.
- Overexpression of miR‑338‑3p and knockdown of NOVA1 in RB cells.
- Dual-luciferase reporter assay and rescue experiments.
Main Results:
- Overexpression of miR‑338‑3p inhibited RB cell proliferation, migration, and invasion, while promoting apoptosis.
- Knockdown of NOVA1 yielded similar tumor-suppressive effects.
- miR‑338‑3p directly targets and binds to NOVA1.
Conclusions:
- miR‑338‑3p functions as a tumor suppressor in RB by targeting the oncogene NOVA1.
- The miR‑338‑3p/NOVA1 axis represents a potential therapeutic target for RB treatment.
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