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Nerve growth factor interacts with CHRM4 and promotes neuroendocrine differentiation of prostate cancer and

Wei-Yu Chen1,2, Yu-Ching Wen3,4, Shian-Ren Lin5

  • 1Department of Pathology, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan. 1047@tmu.edu.tw.

Communications Biology
|January 5, 2021
PubMed

Insights

Nerve growth factor (NGF) drives neuroendocrine prostate cancer (NEPC) progression by upregulating cholinergic receptor muscarinic 4 (CHRM4) after androgen-deprivation therapy (ADT). Targeting the NGF-CHRM4 axis may offer new NEPC therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Urology

Background:

  • Nerve growth factor (NGF) promotes cancer progression, but its role in neuroendocrine prostate cancer (NEPC) is not well understood.
  • Androgen-deprivation therapy (ADT) is a common treatment for prostate cancer, but it can lead to NEPC development.

Purpose of the Study:

  • To investigate the functional role and regulatory mechanisms of NGF in NEPC development.
  • To explore the NGF-CHRM4 axis as a potential therapeutic target for NEPC.

Main Methods:

  • Investigated ZBTB46-mediated transcriptional activation of NGF.
  • Examined NGF interaction with cholinergic receptor muscarinic 4 (CHRM4) in NEPC differentiation.
  • Assessed the impact of NGF blockade and knockdown on CHRM4-mediated signaling.
  • Correlated CHRM4 and NGF levels with patient outcomes in high-grade and small-cell NEPC (SCNC).

Main Results:

  • Androgen-deprivation therapy (ADT)-stimulated ZBTB46 upregulates NGF.
  • NGF interacts with CHRM4 to regulate NEPC differentiation and AKT-MYCN signaling.
  • NGF blockade and knockdown inhibit CHRM4-mediated NEPC differentiation.
  • CHRM4 stimulation correlates with ADT resistance and increased NGF in SCNC patients.

Conclusions:

  • The NGF-CHRM4 axis plays a critical role in NEPC development, driven by ZBTB46 upregulation and CHRM4 accumulation post-ADT.
  • Targeting the NGF-CHRM4 pathway presents a promising therapeutic strategy to impede NEPC progression.

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