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The stem cell niche is the dynamic microenvironment where stem cells reside. Inside these niches, the cells may remain undifferentiated, undergo high self-renewal, or become lineage-specific progenitors. Stem cells coexist with other niche cells, such as stromal cells. They also interact closely with the ECM. Cell-cell and cell-matrix communication occur via adhesion molecules or soluble factors that signal the stem cells and determine their fate. Stromal cells also provide survival signals to...
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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...
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Related Experiment Video

Updated: Feb 5, 2026

The Organoid Reconstitution Assay ORA for the Functional Analysis of Intestinal Stem and Niche Cells
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An intestinal stem cell niche in

Ayesha T Chawla1, Agnes D Cororaton2, Michael O Idowu3,4

  • 1VCU Wright Center for Clinical and Translational Research, Virginia Commonwealth University, Richmond, VA 23298, USA.

Oncotarget
|September 11, 2018
PubMed
Summary
This summary is machine-generated.

C-terminal binding protein 2 (CtBP2) drives intestinal polyposis. Reducing CtBP2 levels or inhibiting its activity significantly decreased tumor-initiating cells and polyps in mouse models, supporting CtBP-targeted therapies for Apc-mutated cancers.

Keywords:
adenomatous polyposisc terminal binding proteintumor initiating cells

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • C-terminal binding protein 2 (CtBP2) is implicated in driving intestinal polyposis, particularly in the Apcmin mouse model relevant to human Familial Adenomatous Polyposis.
  • Understanding CtBP2's function in adenoma formation is crucial for developing effective CtBP-targeted therapies for Apc-mutated cancers.

Purpose of the Study:

  • To investigate the role of CtBP2 gene dosage and activity in intestinal polyposis and tumor-initiating cell (TIC) populations.
  • To evaluate the therapeutic potential of a CtBP inhibitor in preclinical models of Apc-mutated neoplasia.

Main Methods:

  • Analysis of intestinal epithelia in ApcminCtbp2+/- mice to assess TIC populations and CtBP2 localization.
  • Treatment of Apcmin mice with the CtBP inhibitor 4-chloro-hydroxyimino phenylpyruvate (4-Cl-HIPP) to evaluate its effect on TIC populations and polyposis.

Main Results:

  • Reduced CtBP2 levels (ApcminCtbp2+/-) significantly decreased intestinal TIC populations.
  • CtBP2 mislocalization to the cytoplasm in intestinal crypt stem cells correlated with lower CD133 expression and reduced polyp burden.
  • CtBP inhibitor 4-Cl-HIPP administration downregulated TIC populations and decreased intestinal polyposis in Apcmin mice.

Conclusions:

  • A critical link exists between intestinal polyposis, TIC populations, and CtBP2 gene dosage or activity.
  • Targeting CtBP demonstrates therapeutic promise for the treatment or prevention of Apc-mutated neoplasia.