Related Experiment Video
Updated: Jan 2, 2026

Reconstruct Human Retinoblastoma In Vitro
Published on: October 11, 2022
NRAS Contributes to Retinoblastoma Progression Through SNHG16/miR-183-5p/NRAS Regulatory Network
Guangli Sun1, Gang Su2, Fang Liu1
1Department of Ophthalmology, The First Affiliated Hospital of Zhengzhou University, Henan, People's Republic of China.
Purpose:
The oncogene of wild type neuroblastoma RAS viral oncogene homolog (NRAS) has been found to involve in the tumorigenesis of cancers. However, the role of NRAS in retinoblastoma (RB) progression remains largely unknown.
Methods:
The expression levels of NRAS, miR-183-5p and small nucleolar RNA host gene 16 (SNHG16) were measured using quantitative real-time polymerase chain reaction assay or Western blot assay, respectively. Cell proliferation and apoptosis were analyzed with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay or flow cytometry, respectively. Transwell assay was used to determine cell migration and invasion abilities. The interaction between miR-183-5p and NRAS or SNHG16 was analyzed using bioinformatics analysis and dual-luciferase reporter assay.
Results:
NRAS was elevated in RB tissues and cell lines, knockdown of NRAS could inhibit proliferation, migration and invasion but induced apoptosis in vitro and suppressed tumor growth in vivo. NRAS was confirmed to be a target of miR-183-5p and was negatively regulated by miR-183-5p in RB cells. Moreover, overexpressed NRAS reversed miR-183-5p mediated inhibition on RB cell progression. Besides that, SNHG16 directly interacted with miR-183-5p and reduced miR-183-5p expression in RB cells. The suppression of RB cell progression induced by SNHG16 silencing could be partially attenuated by the inhibition of miR-183-5p. Besides that, SNHG16 could regulate NRAS expression through competitively binding to miR-183-5p in RB cells.
Conclusion:
NRAS functioned as an oncogene to contribute to RB progression by SNHG16/miR-183-5p/NRAS regulatory network, indicating a novel and promising therapeutic target for RB.
Insights
Neuroblastoma RAS viral oncogene homolog (NRAS) acts as an oncogene in retinoblastoma (RB) progression. The SNHG16/miR-183-5p/NRAS network highlights NRAS as a potential therapeutic target for RB.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- The neuroblastoma RAS viral oncogene homolog (NRAS) is implicated in various cancers.
- The specific role of NRAS in retinoblastoma (RB) progression is not well understood.
Purpose of the Study:
- To investigate the function of NRAS in retinoblastoma (RB) progression.
- To elucidate the regulatory network involving NRAS, miR-183-5p, and SNHG16 in RB.
Main Methods:
- Quantitative real-time PCR and Western blot assays were used to measure expression levels of NRAS, miR-183-5p, and SNHG16.
- Cell proliferation, apoptosis, migration, and invasion were assessed using MTT assays, flow cytometry, and Transwell assays.
- Bioinformatics and dual-luciferase reporter assays were employed to analyze molecular interactions.
Main Results:
- Elevated NRAS expression was observed in RB tissues and cell lines; NRAS knockdown inhibited proliferation, migration, and invasion while inducing apoptosis.
- NRAS was identified as a direct target of miR-183-5p, with NRAS negatively regulated by miR-183-5p.
- SNHG16 directly interacted with miR-183-5p, reducing its expression and subsequently influencing NRAS levels, forming a regulatory network.
Conclusions:
- NRAS functions as an oncogene promoting RB progression through the SNHG16/miR-183-5p/NRAS regulatory axis.
- This regulatory network presents a novel and promising therapeutic target for retinoblastoma.
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