Evidence map›Paper›PMID 29453334›Full record

ArticleScientific reports2018

β-catenin-independent regulation of Wnt target genes by RoR2 and ATF2/ATF4 in colon cancer cells.

Oksana Voloshanenko, Uwe Schwartz, Dominique Kranz, Benedikt Rauscher, Michael Linnebacher, Iris Augustin, Michael Boutros

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 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

42 citing papers in PubMed, 50 citations in OpenAlex.

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  15. Injury-induced MAPK activation triggers body axis formation inProceedings of the National Academy of Sciences of the United States of America · 2022
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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

7 authors at 4 institutions in 1 country.

Oksana VoloshanenkoGerman Cancer Research Center (DKFZ), Division of Signaling and Functional Genomics and Heidelberg University, Department of Cell and Molecular Biology, Medical Faculty Mannheim, 69120, Heidelberg, Germany. o.voloshanenko@dkfz.de.
Uwe SchwartzGerman Cancer Research Center (DKFZ), Division of Signaling and Functional Genomics and Heidelberg University, Department of Cell and Molecular Biology, Medical Faculty Mannheim, 69120, Heidelberg, Germany.
Dominique KranzGerman Cancer Research Center (DKFZ), Division of Signaling and Functional Genomics and Heidelberg University, Department of Cell and Molecular Biology, Medical Faculty Mannheim, 69120, Heidelberg, Germany.
Benedikt RauscherGerman Cancer Research Center (DKFZ), Division of Signaling and Functional Genomics and Heidelberg University, Department of Cell and Molecular Biology, Medical Faculty Mannheim, 69120, Heidelberg, Germany.
Michael LinnebacherGeneral Surgery, Section of Molecular Oncology and Immunotherapy, University of Rostock, 18057, Rostock, Germany.
Iris AugustinGerman Cancer Research Center (DKFZ), Division of Signaling and Functional Genomics and Heidelberg University, Department of Cell and Molecular Biology, Medical Faculty Mannheim, 69120, Heidelberg, Germany.
Michael BoutrosGerman Cancer Research Center (DKFZ), Division of Signaling and Functional Genomics and Heidelberg University, Department of Cell and Molecular Biology, Medical Faculty Mannheim, 69120, Heidelberg, Germany. m.boutros@dkfz.de.
German Cancer Research Center · DEUniversity Hospital Heidelberg · DEHeidelberg University · DEUniversity of Rostock · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wnt signaling is an evolutionarily conserved signaling route required for development and homeostasis. While canonical, β-catenin-dependent Wnt signaling is well studied and has been linked to many forms of cancer, much less is known about the role of non-canonical, β-catenin-independent Wnt signaling. Here, we aimed at identifying a β-catenin-independent Wnt target gene signature in order to understand the functional significance of non-canonical signaling in colon cancer cells. Gene expression profiling was performed after silencing of key components of Wnt signaling pathway and an iterative signature algorithm was applied to predict pathway-dependent gene signatures. Independent experiments confirmed several target genes, including PLOD2, HADH, LCOR and REEP1 as non-canonical target genes in various colon cancer cells. Moreover, non-canonical Wnt target genes are regulated via RoR2, Dvl2, ATF2 and ATF4. Furthermore, we show that the ligands Wnt5a/b are upstream regulators of the non-canonical signature and moreover regulate proliferation of cancer cells in a β-catenin-independent manner. Our experiments indicate that colon cancer cells are dependent on both β-catenin-dependent and -independent Wnt signaling routes for growth and proliferation.

Indexed as

Activating Transcription Factor 2Activating Transcription Factor 4beta CateninCell Line, TumorCell ProliferationColonic NeoplasmsGene Expression Regulation, NeoplasticHumansReceptor Tyrosine Kinase-like Orphan ReceptorsWnt ProteinsWnt Signaling PathwayActivating Transcription Factor 2Activating Transcription Factor 4ATF2 protein, humanATF4 protein, humanbeta CateninReceptor Tyrosine Kinase-like Orphan ReceptorsROR2 protein, humanWnt Proteins

Identifiers

PMID29453334
PMCPMC5816634
OpenAlexW2803901658

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.