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Related Experiment Video

Updated: Apr 29, 2026

An Orthotopic Murine Model of Human Prostate Cancer Metastasis
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ERRγ impedes neuroendocrine prostate cancer development.

Ting Li1,2,3, Catherine R Dufour4, Lingwei Han4,5

  • 1Goodman Cancer Institute, McGill University, Montréal, Québec H3A 1A3, Canada; vincent.giguere@mcgill.ca tingli@um.edu.mo.

Genes & Development
|October 29, 2025
PubMed
Summary

Loss of nuclear receptor ERRγ drives neuroendocrine prostate cancer (NEPC) progression. Restoring ERRγ function suppresses tumor growth, offering new therapeutic strategies for this lethal prostate cancer subtype.

Keywords:
ChIP-seqEZH2NEPCPROX1RETRNA-seqadenocarcinomalineage plasticitymetabolismnuclear receptortranscription

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Neuroendocrine prostate cancer (NEPC) is a lethal subtype of castration-resistant prostate cancer (CRPC).
  • The molecular drivers of CRPC progression to NEPC are not fully understood.
  • Effective treatments for NEPC are urgently needed.

Purpose of the Study:

  • To investigate the role of the nuclear receptor ERRγ in prostate cancer progression to NEPC.
  • To identify potential therapeutic targets for NEPC based on ERRγ function.

Main Methods:

  • Utilized a Pten-deficient mouse model of prostate adenocarcinoma.
  • Employed advanced cellular and xenograft models of human prostate cancer.
  • Investigated ERRγ gain-of-function and loss-of-function effects.
  • Analyzed neuroendocrine transcriptional programs and metabolic reprogramming.
  • Evaluated combined pharmacological inhibition of EZH2 and RET kinase.

Main Results:

  • Loss of ERRγ promotes neuroendocrine differentiation in prostate adenocarcinoma.
  • ERRγ gain of function reverses NEPC features, suppresses tumor growth, and alters metabolism.
  • ERRγ deficiency activates a neuroendocrine transcriptional program.
  • Combined EZH2 and RET kinase inhibition effectively targets ERRγ-deficient NEPC cells and organoids.

Conclusions:

  • ERRγ downregulation is a key facilitator of prostate cancer adeno-to-neuroendocrine transformation.
  • Targeting the vulnerability created by ERRγ deficiency offers a promising therapeutic strategy for NEPC.
  • Pharmacological inhibition of EZH2 and RET kinase presents a potential treatment for NEPC.