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Updated: Dec 20, 2025

Isolation, Enrichment, and Maintenance of Medulloblastoma Stem Cells
06:32

Isolation, Enrichment, and Maintenance of Medulloblastoma Stem Cells

Published on: September 1, 2010

16.7K

FHOD3 promotes carcinogenesis by regulating RhoA/ROCK1/LIMK1 signaling pathway in medulloblastoma

J Yu1, W Shi1, R Zhao1

  • 1Department of Neurosurgery, Children's Hospital of Fudan University, 399 Wanyuan Road, Shanghai, 201102, China.

Clinical & Translational Oncology : Official Publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
|May 25, 2020
PubMed
Abstract

Insights

FHOD3 gene expression is elevated in pediatric medulloblastoma, correlating with poorer survival. Inhibiting FHOD3 reduces tumor cell growth, migration, and survival, suggesting it as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Medulloblastoma (MB) is a common pediatric brain cancer with poor survival rates due to limited effective treatments.
  • Understanding the molecular mechanisms driving MB is crucial for developing novel therapeutic strategies.
  • The gene FHOD3's role in MB pathogenesis remains largely unexplored, despite its known involvement in other cancers and development.

Purpose of the Study:

  • To investigate the expression and functional role of FHOD3 in medulloblastoma.
  • To determine the association between FHOD3 expression and patient survival outcomes.
  • To elucidate the molecular pathways regulated by FHOD3 in medulloblastoma cells.

Main Methods:

  • Quantitative real-time PCR (RT-qPCR) and immunohistochemistry (IHC) to assess FHOD3 expression.
  • Kaplan-Meier (K-M) analysis to correlate FHOD3 levels with patient survival.
  • RNA interference (RNAi) to knockdown FHOD3, followed by cell counting kit-8 (CCK-8), colony formation, Transwell assays, and flow cytometry (FACs) to evaluate cellular functions.
  • Western blotting to analyze the phosphorylation status of RhoA, ROCK1, and LIMK1.

Main Results:

  • FHOD3 expression was significantly upregulated (1.5-fold) in medulloblastoma tissues compared to controls, confirmed by IHC.
  • Higher FHOD3 expression correlated with significantly shorter overall survival in MB patients (13.0 vs. 43.8 months).
  • Knockdown of FHOD3 markedly reduced medulloblastoma cell proliferation, colony formation, migration, and invasion, while increasing apoptosis. FHOD3 knockdown also decreased RhoA/ROCK1/LIMK1 pathway activation.

Conclusions:

  • FHOD3 is overexpressed in medulloblastoma and is associated with poor patient survival.
  • FHOD3 plays a critical role in promoting medulloblastoma cell proliferation, growth, survival, and metastasis.
  • FHOD3 may exert its oncogenic functions by regulating the RhoA/ROCK1/LIMK1 signaling pathway, presenting a potential therapeutic target.
Keywords:
FHOD3MedulloblastomaROCK1RhoA

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