Evidence map›Paper›PMID 40619482›Full record

ArticleScientific reports2025

CDX2 loss in colorectal cancer cells is associated with invasive properties and tumor budding.

Nils Bodmer, Kristin Uth, Rina Mehmeti, Cansaran Saygili Demir, Deborah Stroka, Nassim Ghaffari-Tabrizi-Wizsy, Alessandro Lugli, Olivier de Wever, Inti Zlobec, Mario P Tschan

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Nils BodmerInstitute of Tissue Medicine and Pathology, University of Bern, Murtenstrasse 31, 3008, Bern, Switzerland.
Kristin UthInstitute of Tissue Medicine and Pathology, University of Bern, Murtenstrasse 31, 3008, Bern, Switzerland.
Rina MehmetiInstitute of Tissue Medicine and Pathology, University of Bern, Murtenstrasse 31, 3008, Bern, Switzerland.
Cansaran Saygili DemirInstitute of Tissue Medicine and Pathology, University of Bern, Murtenstrasse 31, 3008, Bern, Switzerland.
Deborah StrokaDepartment of Visceral Surgery and Medicine, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
Nassim Ghaffari-Tabrizi-WizsyDivision of Immunology, Research Unit CAM Lab, Otto Loewi Research Center, Medical University of Graz, Graz, Austria.
Alessandro LugliInstitute of Tissue Medicine and Pathology, University of Bern, Murtenstrasse 31, 3008, Bern, Switzerland.
Olivier de WeverCancer Research Institute Ghent (CRIG), Ghent University, Ghent, Belgium.
Inti ZlobecInstitute of Tissue Medicine and Pathology, University of Bern, Murtenstrasse 31, 3008, Bern, Switzerland. inti.zlobec@unibe.ch.
Mario P TschanInstitute of Tissue Medicine and Pathology, University of Bern, Murtenstrasse 31, 3008, Bern, Switzerland. mario.tschan@unibe.ch.

Funding

Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung 31003A_166578/1Swiss Government Excellence Scholarship ESKAS, nr. 2021.0019 / Kosovo / OP
6 · The paper itself

Abstract

In colorectal cancer (CRC), tumor buds (TB) are observed histologically as single tumor cell or small tumor cell clusters located mainly at the advancing tumor edge. TB are a marker of poor prognosis and correlate with metastatic disease in CRC patients. They often lack expression of CDX2 and overexpress markers involved in epithelial-mesenchymal transition (EMT). We evaluated the function of CDX2 in CRC proliferation and migration using CRISPR/Cas9 technology and demonstrated a possible link to tumor dissociation and tumor budding. Knocking out CDX2 in CRC cell lines significantly increased migration. Importantly, the observed phenotypes could be rescued by re-expressing CDX2 and by specific CRISPR synergistic activation mediator (SAM) of endogenous CDX2 in CDX2 low expressing CRC cell lines. Multiplex immunofluorescence (mIF) analysis of primary tumor regions compared to TB in a CDX2-positive CRC patient sample as well as patient derived xenografts (PDX) revealed significantly lower CDX2 expression and correlating E-cadherin levels in TB compared to primary tumor regions, in both models. Accordingly, increased invasiveness of CRC CDX2 knockout cells was seen in ex ovo xenografts. Taken together, our results provide further insight into the function of CDX2 in preventing CRC cell migration, tumor budding and tumor aggressiveness.

Indexed as

CDX2 Transcription FactorColorectal NeoplasmsAnimalsCadherinsCell Line, TumorCell MovementCell ProliferationCRISPR-Cas SystemsEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMiceNeoplasm InvasivenessCadherinsCDX2 protein, humanCDX2 Transcription FactorCDX2Cell migrationColorectal cancerEMTTumor budding

Identifiers

PMID40619482
PMCPMC12230109

What OpenQuestion holds

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Registered trials

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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.