RBM5 Acts as Tumor Suppressor in Medulloblastoma through Regulating Wnt/β-Catenin Signaling

Jianzhong Yu1, Guangchun Ji2, Wei Shi1

  • 1Department of Neurosurgery, Children's Hospital of Fudan University, Shanghai, China.

European Neurology
|July 2, 2020
PubMed
Abstract

Insights

RNA-binding protein 5 (RBM5) acts as a tumor suppressor in medulloblastoma (MB). Lower RBM5 expression correlates with reduced overall survival in MB patients, suggesting a role in disease progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The tumor suppressor role of RNA-binding protein 5 (RBM5) is established in lung and breast cancers.
  • Its specific function in medulloblastoma (MB) pathogenesis is not well understood.
  • Previous exome sequencing identified RBM5 mutations in 40 MB patients.

Purpose of the Study:

  • To investigate the role of RBM5 in medulloblastoma (MB) progression.
  • To analyze the association between RBM5 expression levels and patient survival.
  • To determine the impact of RBM5 on MB cell behavior and signaling pathways.

Main Methods:

  • Immunohistochemistry was used to analyze RBM5 expression in 40 MB patient tissues.
  • Kaplan-Meier analysis assessed the correlation between RBM5 expression and overall survival (OS).
  • RBM5 knockdown and overexpression experiments in Daoy and ONS-76 cells evaluated effects on proliferation, migration, and Wnt/β-catenin signaling.

Main Results:

  • RBM5 mRNA and protein levels were significantly lower in MB tissues compared to normal controls.
  • Low RBM5 expression was significantly associated with reduced OS (p = 0.034).
  • RBM5 knockdown increased proliferation in MB cells, while RBM5 overexpression inhibited proliferation and migration in vitro. Wnt/β-catenin pathway components were altered upon RBM5 modulation.

Conclusions:

  • RBM5 functions as a tumor suppressor in medulloblastoma (MB).
  • Reduced RBM5 expression is linked to poorer overall survival in MB patients.
  • RBM5 appears to regulate MB progression, potentially through the Wnt/β-catenin signaling pathway.

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