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Related Concept Videos

Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

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...
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

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...
Renewal of Intestinal Stem Cells01:23

Renewal of Intestinal Stem Cells

The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the goblet,...

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Related Experiment Video

Updated: May 21, 2026

Combined Conditional Knockdown and Adapted Sphere Formation Assay to Study a Stemness-Associated Gene of Patient-derived Gastric Cancer Stem Cells
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Combined Conditional Knockdown and Adapted Sphere Formation Assay to Study a Stemness-Associated Gene of Patient-derived Gastric Cancer Stem Cells

Published on: May 9, 2020

Transcriptomic study of dormant gastrointestinal cancer stem cells.

Shimpei Nishikawa1, Dyah Laksmi Dewi, Hideshi Ishii

  • 1Department of Frontier Science for Cancer and Chemotherapy, Osaka University, Graduate School of Medicine, Suita, Osaka 565-0871, Japan.

International Journal of Oncology
|June 28, 2012
PubMed
Summary

Dormant cancer stem cells (CSCs) in gastrointestinal cancer resist therapy by employing error-prone DNA repair. Understanding their epigenetic regulation offers new avenues for targeted cancer treatments.

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Area of Science:

  • Gastrointestinal cancer research
  • Cancer stem cell biology
  • Epigenetics and molecular oncology

Background:

  • Cancer stem cells (CSCs) in gastrointestinal cancer exist in dormant and proliferating states.
  • This coexistence contributes to chemoradiation resistance and tumor relapse.
  • Dormant CSCs (CD13+/CD90-) survive hypoxic conditions and exhibit limited proliferation, while proliferating CSCs (CD13-/CD90+) are chemo-sensitive.

Purpose of the Study:

  • To investigate the epigenetic mechanisms driving the malignant behavior of dormant CSCs.
  • To understand how dormancy contributes to therapy resistance and cancer progression.
  • To identify potential molecular targets for novel cancer therapies.

Main Methods:

  • Transcriptomic analysis to elucidate epigenetic regulation in dormant CSCs.
  • Investigation of DNA repair mechanisms (non-homologous end-joining vs. homologous recombination) in different CSC populations.
  • Analysis of signaling pathways including EZH2, TP53, and microRNA101.

Main Results:

  • Dormant CSCs (CD13+) predominantly utilize error-prone non-homologous end-joining for DNA repair after damage.
  • Proliferating CSCs (CD13-) show high-fidelity homologous recombination.
  • Transcriptomic studies revealed simultaneous activation of EZH2- and TP53-related pathways in dormant CSCs, regulated by microRNA101.

Conclusions:

  • Dormancy is a critical protective mechanism for CSCs against therapy.
  • Epigenetic dysregulation, specifically involving microRNA101, EZH2, and TP53, underlies the malignant behavior of dormant CSCs.
  • A pharmacogenomic approach targeting these pathways holds promise for developing novel molecular therapies against gastrointestinal cancer.