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Updated: Feb 10, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
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A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer

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Molecular drivers of metastatic castrate-resistant prostate cancer: New roads to resistance

Phoebe A Huang1, Douglas K Price1, William D Figg1

  • 1a Genitourinary Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Bethesda , MD , USA.

Cancer Biology & Therapy
|May 15, 2018
PubMed

Insights

Loss of SPDEF and gain of TGFBI drives metastatic castrate-resistant prostate cancer (mCRPC) via a novel androgen-mediated axis. Inhibiting androgen signaling may paradoxically promote mCRPC by suppressing tumor-suppressive androgen receptor functions.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Metastatic castrate-resistant prostate cancer (mCRPC) involves complex signaling pathways.
  • The interplay between growth signaling and androgen receptor (AR) function in mCRPC is not fully understood.
  • Androgen deprivation therapy (ADT) is a standard treatment, but resistance mechanisms are critical.

Purpose of the Study:

  • To elucidate novel signaling mechanisms driving mCRPC progression.
  • To investigate the role of SPDEF and TGFBI in AR signaling and metastasis.
  • To understand how AR function influences resistance to ADT.

Main Methods:

  • Analysis of signaling pathways in prostate cancer models.
  • Investigating the functional roles of SPDEF and TGFBI.
  • Studying the impact of androgen receptor signaling on metastasis and therapy resistance.

Main Results:

  • A novel androgen-mediated signaling axis involving loss of SPDEF and gain of TGFBI was identified.
  • This axis promotes metastasis in prostate cancer.
  • The findings suggest that SPDEF loss and TGFBI gain contribute to resistance to androgen deprivation therapy.
  • Androgen receptor signaling plays a complex role, with potential tumor-suppressive functions.

Conclusions:

  • The identified SPDEF/TGFBI axis represents a new mechanism in mCRPC development.
  • Therapeutic strategies targeting androgen signaling need careful consideration due to potential adverse effects on AR tumor-suppressive functions.
  • Understanding this axis may lead to improved treatments for advanced prostate cancer.
Keywords:
ADT resistanceAndrogen receptorSPDEFTGFBIepithelial-mesenchymal transitionmCRPCreceptor signalingtumor suppressor

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