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.

Oncotargets and Therapy
|December 13, 2019
PubMed
Abstract

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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