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Area of Science:

  • Stem cell biology
  • Epithelial biology
  • Cell signaling

Background:

  • Glandular epithelia, such as mammary and prostate, consist of basal cells (BCs) and luminal cells (LCs).
  • Adult basal stem cells (BSCs) are typically unipotent but can regain multipotency during regeneration or oncogene activation.
  • The mechanism restricting BSC multipotency under normal physiological conditions is currently unknown.

Purpose of the Study:

  • To investigate the mechanism that restricts basal stem cell (BSC) multipotency in glandular epithelia.
  • To identify the cellular and molecular players involved in maintaining lineage fidelity.

Main Methods:

  • Investigated BSC multipotency in vivo (mice) and in vitro (organoids) following luminal cell (LC) ablation.
  • Utilized bulk and single-cell RNA sequencing to analyze gene expression changes in BSCs.
  • Predicted ligand-receptor interactions from single-cell data to identify signaling pathways.

Main Results:

  • LC ablation reactivated BSC multipotency, inducing a hybrid basal and luminal cell differentiation program.
  • Tumor necrosis factor (TNF), secreted by LCs, was identified as a key inhibitor of BSC multipotency.
  • Notch, Wnt, and EGFR pathways were activated upon LC ablation; their inhibition or TNF stimulation blocked BSC multipotency.

Conclusions:

  • Heterotypic communication between LCs and BCs is crucial for maintaining lineage fidelity in glandular epithelial stem cells.
  • TNF signaling from LCs actively suppresses BSC multipotency under normal physiological conditions.
  • Understanding this communication provides insights into stem cell regulation and potential therapeutic targets.