Evidence map›Paper›PMID 30858446›Full record

ArticleScientific reports2019

Loss of Neogenin1 in human colorectal carcinoma cells causes a partial EMT and wound-healing response.

Vishal Chaturvedi, Alexandre Fournier-Level, Helen M Cooper, Michael J Murray

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 24% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Predictive capacity for local disease control of neogenin-1 (NEO1) transcriptional expression in patients with head and neck squamous cell carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
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  10. Prognostic impact of cancer stem cell markersAmerican journal of translational research · 2020
    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

4 authors at 2 institutions in 1 country.

Vishal ChaturvediSchool of Biosciences, The University of Melbourne, Melbourne, Victoria, 3010, Australia.
Alexandre Fournier-LevelSchool of Biosciences, The University of Melbourne, Melbourne, Victoria, 3010, Australia.
Helen M CooperThe University of Queensland, Queensland Brain Institute, Brisbane, Queensland, 4072, Australia.
Michael J MurraySchool of Biosciences, The University of Melbourne, Melbourne, Victoria, 3010, Australia. murraym@unimelb.edu.au.
University of Melbourne · AUUniversity of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neogenin1 (NEO1) is a receptor of the Deleted in Colorectal Carcinoma (DCC)/Frazzled/UNC-40 family, which regulates axon guidance but can also stabilize epithelial adherens junctions. NEO1 and DCC are also tumor suppressors that can inhibit metastasis by acting as dependence receptors. Given the role of NEO1 in maintaining adherens junctions we tested whether loss of NEO1 also promoted metastasis via an epithelial mesenchymal transition (EMT). Loss of NEO1 disrupted zonula adherens but tight junctions were unaffected. Neo1-depleted epithelial cells exhibited a more migratory morphology, had reduced F-actin rich stress-fibres and more basal lamellipodia. Microtubule density was decreased while microtubule outgrowth was faster. Live imaging showed that Neo1-depleted epithelial islands had increased lateral movement. Western blots and immunostaining revealed increased expression of mesenchymal markers such as Fibronectin and MMP1. Furthermore, RNA-seq analysis showed a striking decrease in expression of genes associated with oxidative phosphorylation, and increased expression of genes associated with EMT, locomotion, and wound-healing. In summary, loss of NEO1 in intestinal epithelial cells produces a partial EMT response, based on gene expression, cellular morphology and behaviour and cytoskeletal distribution. These results suggest that loss of NEO1 in carcinomas may contribute to metastasis by promoting a partial EMT and increased motility.

Indexed as

Epithelial-Mesenchymal TransitionWound HealingAdherens JunctionsApoptosisCaco-2 CellsCell MovementCell RespirationColorectal NeoplasmsEpithelial CellsExtracellular MatrixGene Expression RegulationGene Knockdown TechniquesGenome, HumanHumansMesodermMicrotubule-Associated ProteinsMAPRE1 protein, humanMicrotubule-Associated ProteinsNEO1 protein, humanNerve Tissue ProteinsReceptors, Cell Surface

Identifiers

PMID30858446
PMCPMC6411945
OpenAlexW2921949557

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.