ZNRD1-AS1 knockdown alleviates malignant phenotype of retinoblastoma through miR-128-3p/BMI1 axis

Guanghua Yang1, Chen Zeng1, Yang Liu2

  • 1First Department of Oncology, Zhumadian Central Hospital Zhumadian, Henan, China.

Abstract

Insights

Long non-coding RNA ZNRD1-AS1 promotes retinoblastoma progression by sponging miR-128-3p and up-regulating BMI1. Knockdown of ZNRD1-AS1 inhibits retinoblastoma cell malignancy and tumor growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • ZNRD1-AS1 is implicated in various cancers, but its role in retinoblastoma remains unclear.
  • Understanding ZNRD1-AS1's function is crucial for developing novel retinoblastoma therapies.

Purpose of the Study:

  • To investigate the role and mechanism of ZNRD1-AS1 in retinoblastoma progression.
  • To explore the regulatory relationship between ZNRD1-AS1, miR-128-3p, and BMI1 in retinoblastoma.

Main Methods:

  • Differential gene expression analysis using GEO database and Limma package.
  • RT-qPCR, dual-luciferase assay, and Western blot to analyze gene expression and interactions.
  • In vitro cell assays (viability, migration, invasion) and in vivo tumor xenograft models to assess functional impact.

Main Results:

  • ZNRD1-AS1 is upregulated in retinoblastoma cytoplasm and acts as a sponge for miR-128-3p, leading to BMI1 upregulation.
  • ZNRD1-AS1 knockdown suppressed retinoblastoma cell malignancy and tumor growth, inhibiting BMI1 and CD34 expression.
  • MiR-128-3p mimic reversed the effects of ZNRD1-AS1 knockdown, while BMI1 partially reversed miR-128-3p's regulatory effects.

Conclusions:

  • ZNRD1-AS1 promotes retinoblastoma progression by sponging miR-128-3p and upregulating BMI1.
  • ZNRD1-AS1 serves as a potential therapeutic target for retinoblastoma.

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