ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Progastrin Promotes Colorectal Cancer Stem Cell-Like Properties via the Receptor PZR.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Slap restricts oncogenic Src-family kinase signaling to maintain colonic epithelial homeostasis.eLife · 2026Article
- A novel therapeutic monoclonal antibody targeting PZR demonstrates potent anti-metastatic efficacy in triple-negative breast cancer.Journal of translational medicine · 2026Article
- Progastrin Promotes Colorectal Cancer Stem Cell-Like Properties via the Receptor PZR.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
23 authors.
Funding
Abstract
The tumor microenvironment promotes cancer progression in part by supporting cancer stem cells (CSC). In colorectal cancer (CRC), progastrin (PG), an orphan growth factor secreted by tumor cells within the tumor and its microenvironment, maintains CSCs by unidentified mechanisms. Here, the orphan receptor Protein Zero-Related protein (PZR) is identified as an essential component of PG activity and demonstrated its utility as a therapeutic target. PZR is essential for growth of PG-expressing tumors, while genetic inactivation in mice of Mpzl1, which encodes PZR, disrupted chemically-induced colon transformation. Mechanistically, PG binds cellular glycosylated and dimeric PZR and promotes SHP2/SRC/β-catenin-dependent CSC-like signaling. Blocking PZR by monoclonal antibodies inhibited PG-dependent expansion of tumoroids derived from murine intestinal tumors and patient-derived CRC cell lines, while in mice, it reduced adenoma formation triggered by Apc loss in stem cells and disrupted the tumor-initiating capacity of PG-expressing CRC cells. High GAST (which encodes PG) and MPZL1 transcript levels in primary colon cancer patients is predictive of worse prognosis. Collectively, these findings support the inhibition of PZR as a potential targeted treatment of PG-expressing CRC.
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Registered trials
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