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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.
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Related Experiment Video

Updated: Apr 13, 2026

Tumor Transplantation for Assessing the Dynamics of Tumor-Infiltrating CD8+ T Cells in Mice
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CDC20 maintains tumor initiating cells.

Qi Xie1, Qiulian Wu1, Stephen C Mack1

  • 1Department of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA.

Oncotarget
|May 5, 2015
PubMed
Summary

Cell division cycle protein 20 (CDC20) drives glioblastoma tumor-initiating cell (TIC) growth by degrading p21CIP1/WAF1. Inhibiting CDC20 halts TIC proliferation and survival, offering a potential therapeutic target for brain tumors.

Keywords:
CDC20cancer stem cellglioblastomagliomatumor initiating cell

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Area of Science:

  • Neuro-oncology
  • Cancer Stem Cell Biology
  • Molecular Oncology

Background:

  • Glioblastoma (GBM) is an aggressive brain tumor characterized by tumor-initiating cells (TICs) or cancer stem cells.
  • Unlike normal neural stem cells, GBM TICs are often proliferative, presenting a vulnerability in cell cycle regulation.

Purpose of the Study:

  • To investigate the role of cell division cycle protein 20 (CDC20) in maintaining glioblastoma tumor-initiating cells (TICs).

Main Methods:

  • Chromatin analysis and immunoblotting to assess CDC20 expression.
  • RNA interference to target CDC20 expression.
  • Assays for TIC proliferation, self-renewal, and in vivo tumor growth.
  • Analysis of apoptosis, cell cycle progression, and protein degradation pathways.

Main Results:

  • CDC20 was highly expressed in TICs compared to non-TICs.
  • Reducing CDC20 inhibited TIC proliferation, self-renewal, and tumor growth by inducing apoptosis and cell cycle arrest.
  • CDC20 promotes TIC survival by degrading p21CIP1/WAF1, a key negative regulator.
  • Inhibition of CDC20 stabilized p21CIP1/WAF1, repressing genes like CDC25C, c-Myc, and Survivin.
  • FOXM1 transcriptionally regulates CDC20 in TICs.

Conclusions:

  • CDC20 is essential for glioblastoma TIC proliferation and survival.
  • CDC20 acts as a crucial link between FOXM1 and p21CIP1/WAF1 pathways.
  • Targeting CDC20 represents a promising therapeutic strategy for glioblastoma.