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Related Concept Videos

Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

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Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
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Flow Cytometry-based Drug Screening System for the Identification of Small Molecules That Promote Cellular Differentiation of Glioblastoma Stem Cells
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Repurposing Clemastine to Target Glioblastoma Cell Stemness.

Michael A Sun1,2,3, Rui Yang1,2, Heng Liu1,2,3

  • 1The Preston Robert Tisch Brain Tumor Center, Duke University Medical Center, Durham, NC 27710, USA.

Cancers
|September 28, 2023
PubMed
Summary

Clemastine, an allergy drug, suppressed glioblastoma stemness by targeting Emopamil Binding Protein (EBP). This repurposed drug shows potential for treating brain tumors by promoting cell differentiation.

Keywords:
Emopamil Binding Protein (EBP)clemastineglioblastomastemness

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Area of Science:

  • Neuro-oncology
  • Cancer Stem Cell Biology
  • Drug Repurposing

Background:

  • Glioblastoma (GBM) progression is driven by brain tumor-initiating cells (BTICs) and tumor cell plasticity.
  • BTICs maintain stemness, contributing to therapeutic resistance and tumor recurrence.

Purpose of the Study:

  • To investigate clemastine's effect on BTIC stemness and propagation.
  • To identify the molecular targets of clemastine in GBM.

Main Methods:

  • Primary BTIC cultures with PDGFRA amplification were treated with clemastine.
  • Gene expression profiling and functional assays were performed.
  • A mouse glioma model was used to assess in vivo efficacy.

Main Results:

  • Clemastine attenuated BTIC stemness and suppressed their propagation.
  • Gene expression changes indicated a more differentiated state in BTICs.
  • Emopamil Binding Protein (EBP) was identified as a key target essential for BTIC propagation.
  • Clemastine treatment was effective in a proneural glioma mouse model.

Conclusions:

  • Clemastine effectively targets GBM stemness by inhibiting EBP.
  • Repurposing non-oncology drugs like clemastine offers a potential therapeutic strategy for GBM.
  • Targeting pathways maintaining GBM stemness and progenitor features is crucial for treatment.