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Intercepting YAP Activation in Prostate Cancer Blocks Neuroendocrine Progression.

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Neuroendocrine prostate cancer (NEPC) develops through interactions between prostate cancer cells and the extracellular matrix, driven by the integrin α2-YAP axis. Targeting this pathway may inhibit NEPC progression and metastasis in patients.

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Area of Science:

  • Oncology
  • Cell Biology
  • Cancer Research

Background:

  • Neuroendocrine prostate cancer (NEPC) emergence correlates with poor prognosis in castration-resistant prostate cancer (CRPC).
  • Androgen deprivation therapy can induce prostate cancer (PC) cell death, potentially promoting NEPC development through interactions with the tumor microenvironment.

Purpose of the Study:

  • To investigate the physical and molecular interactions between prostate cancer cells and extracellular matrix (ECM) that drive NEPC development.
  • To identify therapeutic targets for NEPC and CRPC.

Main Methods:

  • Studied interactions between exocrine (PAC) and neuroendocrine (PNE) prostate cancer cells and decellularized prostate ECM.
  • Assessed the role of integrin α2, YAP, RANK/RANKL, and NF-κB in NEPC invasiveness.
  • Utilized in vitro cell models, in vivo mouse models (castration-naïve and transgenic), and human CRPC organoids.

Main Results:

  • Androgen deprivation promoted PNE cell invasiveness via integrin α2 upregulation and YAP activation, driven by PAC cells and ECM.
  • Inhibition of RANK/RANKL, NF-κB, integrin α2β1, and YAP reduced PNE cell invasiveness.
  • YAP inhibition suppressed NEPC development, metastasis in vivo, and CRPC organoid growth.

Conclusions:

  • The integrin α2-YAP axis is crucial for NEPC development and progression in the context of CRPC.
  • Targeting the integrin α2-YAP axis presents a potential therapeutic strategy for NEPC and CRPC patients undergoing androgen-deprivation therapy.