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Updated: Sep 18, 2025

Evaluating the Differentiation Capacity of Mouse Prostate Epithelial Cells Using Organoid Culture
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Innate immunity and the NF-κB pathway control prostate stem cell plasticity, reprogramming and tumor initiation.

Chen Jiang1, Yura Song1, Sandrine Rorive2

  • 1Laboratory of Stem Cells and Cancer, Université Libre de Bruxelles (ULB), Brussels, Belgium.

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|June 23, 2025
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Deleting Pten in prostate basal cells (BCs) triggers cell plasticity and tumor initiation. Targeting innate immunity pathways like IL-1, JAK-STAT, and NF-κB inhibits this Pten-induced reprogramming, offering new prostate cancer treatment strategies.

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Area of Science:

  • Prostate cancer research
  • Stem cell biology
  • Cancer epigenetics

Background:

  • Prostate epithelium originates from multipotent stem cells, differentiating into lineage-restricted basal and luminal cells in adults.
  • Loss of Pten in basal cells (BCs) can restore multipotency, but mechanisms of BC plasticity and tumor initiation remain unclear.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying basal cell plasticity and prostate tumor initiation following Pten deletion.
  • To identify potential therapeutic targets for prostate cancer based on Pten-driven reprogramming.

Main Methods:

  • Single-cell RNA sequencing and ATAC-seq were employed to analyze cell fate changes after Pten deletion.
  • In situ characterization and pharmacological/genetic inhibition of key signaling pathways were performed.

Main Results:

  • Pten deletion in prostate BCs induced regionalized cell fate reprogramming, characterized by a progression through hillock-like and proximal-like luminal states.
  • This reprogramming was linked to the activation of innate immunity signaling pathways, including interleukin-1, JAK-STAT, and NF-κB.
  • Inhibition of these pathways, either pharmacologically or genetically, effectively blocked Pten-induced BC plasticity and reprogramming.

Conclusions:

  • Pten loss drives prostate basal cell plasticity and tumor initiation via a defined cell fate trajectory.
  • Innate immunity pathways are critical mediators of Pten-driven prostate cancer development.
  • Targeting IL-1, JAK-STAT, and NF-κB pathways presents a promising strategy for prostate cancer prevention and treatment.