Evidence map›Paper›PMID 32203506›Full record

ArticlePLoS genetics2020

The Caenorhabditis elegans homolog of the Evi1 proto-oncogene, egl-43, coordinates G1 cell cycle arrest with pro-invasive gene expression during anchor cell invasion.

Ting Deng, Przemyslaw Stempor, Alex Appert, Michael Daube, Julie Ahringer, Alex Hajnal, Evelyn Lattmann

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

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  18. A developmental gene regulatory network forDevelopment (Cambridge, England) · 2020
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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 2 institutions in 2 countries.

Ting DengInstitute of Molecular Life Sciences, University of Zurich, Winterthurerstrasse, Zürich, Switzerland.ORCID 0000-0002-4820-8535
Przemyslaw StemporThe Gurdon Institute and Department of Genetics, University of Cambridge, Cambridge, United Kingdom.ORCID 0000-0002-9464-7475
Alex AppertThe Gurdon Institute and Department of Genetics, University of Cambridge, Cambridge, United Kingdom.
Michael DaubeInstitute of Molecular Life Sciences, University of Zurich, Winterthurerstrasse, Zürich, Switzerland.
Julie AhringerThe Gurdon Institute and Department of Genetics, University of Cambridge, Cambridge, United Kingdom.ORCID 0000-0002-7074-4051
Alex HajnalInstitute of Molecular Life Sciences, University of Zurich, Winterthurerstrasse, Zürich, Switzerland.ORCID 0000-0002-4098-3721
Evelyn LattmannInstitute of Molecular Life Sciences, University of Zurich, Winterthurerstrasse, Zürich, Switzerland.ORCID 0000-0002-9793-2554
University of Zurich · CHUniversity of Cambridge · GB

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
Cancer Research UK C6946/A14492NIH HHS P40 OD010440Wellcome Trust 092096Wellcome Trust 101863
6 · The paper itself

Abstract

Cell invasion allows cells to migrate across compartment boundaries formed by basement membranes. Aberrant cell invasion is a first step during the formation of metastases by malignant cancer cells. Anchor cell (AC) invasion in C. elegans is an excellent in vivo model to study the regulation of cell invasion during development. Here, we have examined the function of egl-43, the homolog of the human Evi1 proto-oncogene (also called MECOM), in the invading AC. egl-43 plays a dual role in this process, firstly by imposing a G1 cell cycle arrest to prevent AC proliferation, and secondly, by activating pro-invasive gene expression. We have identified the AP-1 transcription factor fos-1 and the Notch homolog lin-12 as critical egl-43 targets. A positive feedback loop between fos-1 and egl-43 induces pro-invasive gene expression in the AC, while repression of lin-12 Notch expression by egl-43 ensures the G1 cell cycle arrest necessary for invasion. Reducing lin-12 levels in egl-43 depleted animals restored the G1 arrest, while hyperactivation of lin-12 signaling in the differentiated AC was sufficient to induce proliferation. Taken together, our data have identified egl-43 Evi1 as an important factor coordinating cell invasion with cell cycle arrest.

Indexed as

AnimalsBasement MembraneCaenorhabditis elegansCaenorhabditis elegans ProteinsCell Cycle CheckpointsCell DifferentiationCell ProliferationG1 Phase Cell Cycle CheckpointsGene ExpressionMDS1 and EVI1 Complex Locus ProteinProto-Oncogene MasProto-Oncogene Proteins c-fosProto-OncogenesReceptors, NotchSignal TransductionTranscription FactorsCaenorhabditis elegans ProteinsFOS-1 protein, C elegansLin-12 protein, C elegansMAS1 protein, humanMDS1 and EVI1 Complex Locus ProteinProto-Oncogene MasProto-Oncogene Proteins c-fosReceptors, NotchTranscription Factors

Identifiers

PMID32203506
PMCPMC7117773
OpenAlexW3012674927

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.