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Updated: Jan 29, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
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Neurotensin and its receptors mediate neuroendocrine transdifferentiation in prostate cancer

Shimiao Zhu1, Hao Tian1, Xiaodan Niu2

  • 1Department of Urology, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, 300211, Tianjin, China.

Oncogene
|February 17, 2019
PubMed

Insights

Neurotensin (NTS) drives castration-resistant prostate cancer (CRPC) with neuroendocrine differentiation (NED) by activating specific receptors. Targeting the NTS signaling pathway may prevent CRPC with NED development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • Castration-resistant prostate cancer (CRPC) with neuroendocrine differentiation (NED) presents a significant therapeutic challenge due to poorly understood mechanisms.
  • Effective treatments for CRPC with NED are urgently needed.

Purpose of the Study:

  • To investigate the role of neurotensin (NTS) in the development of CRPC with NED.
  • To characterize the signaling pathways involved in NTS-mediated neuroendocrine differentiation.

Main Methods:

  • Utilized cell line (LNCaP) and animal models of prostate cancer (PCa) and CRPC with NED.
  • Examined NTS induction by androgen deprivation.
  • Assessed the role of neurotensin receptors (NTSR1, NTSR3) in NED development.
  • Investigated the effect of NTSR1 pathway inhibition on CRPC with NED progression in vivo.

Main Results:

  • Neurotensin (NTS) is acutely induced by androgen deprivation in prostate cancer models.
  • NTS activates neurotensin receptor 1 (NTSR1) and neurotensin receptor 3 (NTSR3) to promote NED.
  • A specific subpopulation of LNCaP cells (CK8+/CK14+) showed increased susceptibility to NTS-induced NED.
  • Inhibition of the NTSR1 pathway effectively prevented NED and castration resistance in vivo.

Conclusions:

  • Neurotensin (NTS) plays a critical role in the development of castration-resistant prostate cancer with neuroendocrine differentiation.
  • Targeting the NTS signaling pathway, particularly NTSR1, offers a potential therapeutic strategy to prevent CRPC with NED.

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