Evidence map›Paper›PMID 31772156›Full record

ArticleCell death & disease2019

DAPK1 loss triggers tumor invasion in colorectal tumor cells.

Sara Steinmann, Philipp Kunze, Chuanpit Hampel, Markus Eckstein, Jesper Bertram Bramsen, Julienne K Muenzner, Birgitta Carlé, Benardina Ndreshkjana, Stephan Kemenes, Pierluigi Gasparini and 8 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 76 citations in OpenAlex.

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  7. DNA methylation biomarkers for predicting lymph node metastasis in colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  8. Current medicinal chemistry · 2025
    Article
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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

18 authors at 4 institutions in 3 countries.

Sara SteinmannExperimental Tumor Pathology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuremberg, Universitaetsstrasse 22, 91054, Erlangen, Germany.ORCID http://orcid.org/0000-0001-9284-1138
Philipp KunzeExperimental Tumor Pathology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuremberg, Universitaetsstrasse 22, 91054, Erlangen, Germany.
Chuanpit HampelExperimental Tumor Pathology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuremberg, Universitaetsstrasse 22, 91054, Erlangen, Germany.
Markus EcksteinInstitute of Pathology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuremberg, Krankenhausstr. 8-10, 91054, Erlangen, Germany.
Jesper Bertram BramsenDepartment of Molecular Medicine, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark.
Julienne K MuenznerExperimental Tumor Pathology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuremberg, Universitaetsstrasse 22, 91054, Erlangen, Germany.
Birgitta CarléInstitute of Biotechnology, Friedrich-Alexander University Erlangen-Nuremberg, Paul-Gordan-Str. 3, 91052, Erlangen, Germany.
Benardina NdreshkjanaExperimental Tumor Pathology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuremberg, Universitaetsstrasse 22, 91054, Erlangen, Germany.
Stephan KemenesExperimental Tumor Pathology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuremberg, Universitaetsstrasse 22, 91054, Erlangen, Germany.
Pierluigi GaspariniDepartment of Cancer Biology and Genetics, College of Medicine, The Ohio State University Comprehensive Cancer Center, Columbus, OH, USA.
Oliver FriedrichInstitute of Biotechnology, Friedrich-Alexander University Erlangen-Nuremberg, Paul-Gordan-Str. 3, 91052, Erlangen, Germany.
Claus AndersenDepartment of Molecular Medicine, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark.ORCID http://orcid.org/0000-0002-7406-2103
Carol GeppertInstitute of Pathology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuremberg, Krankenhausstr. 8-10, 91054, Erlangen, Germany.
Shengbao WangDepartment of Neurosurgery, University Hospital Erlangen-Nuremberg, Schwabachanlage 6, 91054, Erlangen, Germany.
Ilker EyupogluDepartment of Neurosurgery, University Hospital Erlangen-Nuremberg, Schwabachanlage 6, 91054, Erlangen, Germany.
Tobias BäuerleDepartment of Radiology, University Hospital Erlangen-Nuremberg, Maximiliansplatz 1, 91054, Erlangen, Germany.
Arndt HartmannInstitute of Pathology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuremberg, Krankenhausstr. 8-10, 91054, Erlangen, Germany.
Regine Schneider-StockExperimental Tumor Pathology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuremberg, Universitaetsstrasse 22, 91054, Erlangen, Germany. regine.schneider-stock@uk-erlangen.de.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversitätsklinikum Erlangen · DEAarhus University Hospital · DKThe Ohio State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is one of the leading cancer-related causes of death worldwide. Despite the improvement of surgical and chemotherapeutic treatments, as of yet, the disease has not been overcome due to metastasis to distant organs. Hence, it is of great relevance to understand the mechanisms responsible for metastasis initiation and progression and to identify novel metastatic markers for a higher chance of preventing the metastatic disease. The Death-associated protein kinase 1 (DAPK1), recently, has been shown to be a potential candidate for regulating metastasis in CRC. Hence, the aim of the study was to investigate the impact of DAPK1 protein on CRC aggressiveness. Using CRISPR/Cas9 technology, we generated DAPK1-deficient HCT116 monoclonal cell lines and characterized their knockout phenotype in vitro and in vivo. We show that loss of DAPK1 implemented changes in growth pattern and enhanced tumor budding in vivo in the chorioallantoic membrane (CAM) model. Further, we observed more tumor cell dissemination into chicken embryo organs and increased invasion capacity using rat brain 3D in vitro model. The novel identified DAPK1-loss gene expression signature showed a stroma typical pattern and was associated with a gained ability for remodeling the extracellular matrix. Finally, we suggest the DAPK1-ERK1 signaling axis being involved in metastatic progression of CRC. Our results highlight DAPK1 as an anti-metastatic player in CRC and suggest DAPK1 as a potential predictive biomarker for this cancer type.

Indexed as

AnimalsAntigens, NeoplasmCell Adhesion MoleculesCell ProliferationChick EmbryoChorioallantoic MembraneClone CellsColorectal NeoplasmsCRISPR-Cas SystemsDeath-Associated Protein KinasesExtracellular MatrixGene Expression Regulation, NeoplasticGene Knockout TechniquesHCT116 CellsHumansMAP Kinase Signaling SystemAntigens, NeoplasmCell Adhesion MoleculesDAPK1 protein, humanDeath-Associated Protein KinasesTACSTD2 protein, human

Identifiers

PMID31772156
PMCPMC6879526
OpenAlexW2989663721

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.