ArticleCell death & disease2025
Loss of cadherin 17 downregulates LGR5 expression, stem cell properties and drug resistance in metastatic colorectal cancer cells.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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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
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Role of Cadherin 17 (CDH17) in Cancer Progression via Wnt/β-Catenin Signalling Pathway: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2025Pooled it
- Mechanisms and advances of drug resistance in colorectal cancer: A systematic overview of multi-layered regulatory networks.Translational oncology · 2026Review
- A Novel Anti-Cadherin-17 Monoclonal Antibody, CaAntibodies (Basel, Switzerland) · 2026Article
- Cadherin 17 and digestive cancers: from diagnostic to therapeutic opportunities.Journal of experimental & clinical cancer research : CR · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Cadherin 17 (CDH17) plays a crucial role in the metastatic progression of colorectal cancer (CRC) through its interaction with α2β1 integrin and desmocollin 1. To further elucidate the molecular mechanisms involving CDH17 functions in CRC, we examined global expression alterations following CDH17 silencing in various metastatic cell lines. Loss of CDH17 resulted in a marked down-regulation of the intestinal cancer stem cell (CSC) marker LGR5, leading to the inhibition of Wnt/β-catenin signaling, suppression of pluripotency genes such as MYC, and a subsequent reduction in stemness properties. Treatment with CDH17/integrin blocking antibodies produced similar effects, decreasing both, LGR5 expression and Wnt signaling. CDH17 silencing also down-regulated various transporters associated with drug-resistance, including the glutamine-transporter SLC38A5. Consequently, the loss of CDH17 increased sensitivity to 5-FU, irinotecan, oxidative stress and anoikis in CRC cells. Notably, SLC38A5 silencing was necessary for CDH17-driven effects on drug resistance and survival. Pharmacological inhibition of SLC38A5 with amiloride, significantly increased cell sensitivity to 5-FU and irinotecan, and improved mouse survival in metastasis models. In conclusion, CDH17 plays a crucial role in maintaining colorectal cancer cell stemness and chemoresistance via LGR5/Wnt/MYC signaling and SLC38A5 expression. These findings underscore the therapeutic potential of CDH17 targeting in metastatic CRC, and support the use of amiloride for inhibiting liver metastasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.