Evidence map›Paper›PMID 29348601›Full record

ArticleScientific reports2018

Exclusion from spheroid formation identifies loss of essential cell-cell adhesion molecules in colon cancer cells.

Mira Stadler, Martin Scherzer, Stefanie Walter, Silvio Holzner, Karoline Pudelko, Angelika Riedl, Christine Unger, Nina Kramer, Beatrix Weil, Jürgen Neesen and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.4field-weighted citation impact, top 5% of its field
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

51 citing papers in PubMed, 89 citations in OpenAlex.

  1. PRX5 as a critical driver of colorectal cancer stemness and tumorigenicity.Redox report : communications in free radical research · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

12 authors at 4 institutions in 3 countries.

Mira StadlerInstitute of Medical Genetics, Medical University of Vienna, Währinger Straße 10, A-1090, Vienna, Austria.
Martin ScherzerInstitute of Medical Genetics, Medical University of Vienna, Währinger Straße 10, A-1090, Vienna, Austria.
Stefanie WalterInstitute of Medical Genetics, Medical University of Vienna, Währinger Straße 10, A-1090, Vienna, Austria.
Silvio HolznerInstitute of Medical Genetics, Medical University of Vienna, Währinger Straße 10, A-1090, Vienna, Austria.
Karoline PudelkoInstitute of Medical Genetics, Medical University of Vienna, Währinger Straße 10, A-1090, Vienna, Austria.
Angelika RiedlInstitute of Medical Genetics, Medical University of Vienna, Währinger Straße 10, A-1090, Vienna, Austria.
Christine UngerInstitute of Medical Genetics, Medical University of Vienna, Währinger Straße 10, A-1090, Vienna, Austria.
Nina KramerInstitute of Medical Genetics, Medical University of Vienna, Währinger Straße 10, A-1090, Vienna, Austria.
Beatrix WeilInstitute of Medical Genetics, Medical University of Vienna, Währinger Straße 10, A-1090, Vienna, Austria.
Jürgen NeesenInstitute of Medical Genetics, Medical University of Vienna, Währinger Straße 10, A-1090, Vienna, Austria.
Markus HengstschlägerInstitute of Medical Genetics, Medical University of Vienna, Währinger Straße 10, A-1090, Vienna, Austria.
Helmut DolznigInstitute of Medical Genetics, Medical University of Vienna, Währinger Straße 10, A-1090, Vienna, Austria. helmut.dolznig@meduniwien.ac.at.ORCID http://orcid.org/0000-0002-6063-3585
Medical University of Vienna · ATBoehringer Ingelheim (Austria) · ATGerman Cancer Research Center · DEKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many cell lines derived from solid cancers can form spheroids, which recapitulate tumor cell clusters and are more representative of the in vivo situation than 2D cultures. During spheroid formation, a small proportion of a variety of different colon cancer cell lines did not integrate into the sphere and lost cell-cell adhesion properties. An enrichment protocol was developed to augment the proportion of these cells to 100% purity. The basis for the separation of spheroids from non-spheroid forming (NSF) cells is simple gravity-sedimentation. This protocol gives rise to sub-populations of colon cancer cells with stable loss of cell-cell adhesion. SW620 cells lacked E-cadherin, DLD-1 cells lost α-catenin and HCT116 cells lacked P-cadherin in the NSF state. Knockdown of these molecules in the corresponding spheroid-forming cells demonstrated that loss of the respective proteins were indeed responsible for the NSF phenotypes. Loss of the spheroid forming phenotype was associated with increased migration and invasion properties in all cell lines tested. Hence, we identified critical molecules involved in spheroid formation in different cancer cell lines. We present here a simple, powerful and broadly applicable method to generate new sublines of tumor cell lines to study loss of cell-cell adhesion in cancer progression.

Indexed as

Gene Expression Regulation, NeoplasticActinsalpha CateninAntigens, CDCadherinsCell AdhesionCell CommunicationCell Line, TumorCell MovementEpithelial Cell Adhesion MoleculeHCT116 CellsHumansKaryotypingPhenotypeSignal TransductionSpheroids, CellularActinsalpha CateninAntigens, CDCadherinsCDH1 protein, humanEPCAM protein, humanEpithelial Cell Adhesion Molecule

Identifiers

PMID29348601
PMCPMC5773514
OpenAlexW2782732374

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.