MiR-424 suppressed viability and invasion by targeting to the DCLK1 in neuroblastoma

M-F Wan1, N Yang, N-Y Qu

  • 1Department of Pediatrics, The First Affiliated Hospital of Shandong First Medical University, Jinan, China. changkuuhgds83623@163.com.

Abstract

Insights

MicroRNA-424 (miR-424) suppresses neuroblastoma growth and spread by targeting doublecortin like kinase 1 (DCLK1). This newly found miR-424/DCLK1 pathway offers new understanding of neuroblastoma development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Neuroblastoma is a common infant cancer originating from the sympathetic nervous system.
  • MicroRNAs (miRNAs) play crucial roles as oncogenes or tumor suppressors in cancer development.

Purpose of the Study:

  • To investigate the function of specific miRNAs in neuroblastoma pathogenesis.
  • To explore the relationship between miR-424 and its potential targets in neuroblastoma cells.

Main Methods:

  • Cell Counting Kit-8 (CCK-8) and transwell assays were used to assess cell viability and invasion.
  • Western blot analysis was performed to evaluate epithelial-mesenchymal transition (EMT) markers.
  • Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to measure miRNA and gene mRNA levels.

Main Results:

  • MiR-424 was found to be downregulated, while doublecortin like kinase 1 (DCLK1) was upregulated in neuroblastoma tissues and cells.
  • MiR-424 demonstrated tumor-suppressive effects by inhibiting cell viability, invasion, and EMT.
  • MiR-424 directly targeted the 3'-untranslated region (UTR) of DCLK1 mRNA, regulating its expression.

Conclusions:

  • MiR-424 suppresses neuroblastoma cell viability, invasion, and EMT by directly targeting DCLK1 mRNA.
  • The identified miR-424/DCLK1 axis provides novel insights into the molecular mechanisms underlying neuroblastoma development.

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