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Progastrin Promotes Colorectal Cancer Stem Cell-Like Properties via the Receptor PZR.

Julie Nguyen1, Marie Lafitte1, Maud Barbery1

  • 1Equipe Labellisée LIGUE 2020 and FRM 2023, CRBM, Univ Montpellier, CNRS, Montpellier, 34293, France.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|August 3, 2025
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Progastrin (PG) supports colorectal cancer stem cells (CSCs) via the orphan receptor Protein Zero-Related protein (PZR). Targeting PZR with antibodies inhibits tumor growth and could treat PG-expressing colorectal cancer.

Keywords:
cancer stem cellscolon cancermAbreceptorsignalingtargeted therapytyrosine kinase

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • The tumor microenvironment fuels cancer progression by sustaining cancer stem cells (CSCs).
  • In colorectal cancer (CRC), progastrin (PG) maintains CSCs through unknown mechanisms.
  • Identifying PG's receptor is crucial for understanding and targeting CRC progression.

Purpose of the Study:

  • To identify the orphan receptor for progastrin (PG) in colorectal cancer (CRC).
  • To investigate the role of this receptor in PG-mediated CSC maintenance and tumor growth.
  • To evaluate the therapeutic potential of targeting this receptor in CRC.

Main Methods:

  • Genetic inactivation of Mpzl1 (encoding PZR) in mice to assess its role in colon cancer.
  • Investigated PG binding to glycosylated, dimeric Protein Zero-Related protein (PZR).
  • Assessed SHP2/SRC/β-catenin signaling pathways downstream of PG-PZR interaction.
  • Utilized monoclonal antibodies to block PZR in vitro (tumoroids) and in vivo (adenoma formation).

Main Results:

  • Protein Zero-Related protein (PZR) was identified as an essential mediator of PG activity.
  • PG binds to cellular PZR, activating SHP2/SRC/β-catenin signaling, promoting CSC-like properties.
  • Blocking PZR inhibited tumoroid expansion, reduced adenoma formation in mice, and impaired CRC cell tumor-initiating capacity.
  • High transcript levels of GAST (PG) and MPZL1 (PZR) correlate with poor prognosis in CRC patients.

Conclusions:

  • PZR is a critical receptor for progastrin's pro-tumorigenic effects in colorectal cancer.
  • PZR mediates PG-driven CSC maintenance and tumor growth through specific signaling pathways.
  • Inhibiting PZR represents a promising targeted therapeutic strategy for progastrin-expressing CRC.