Evidence map›Paper›PMID 24686166›Full record

ArticleCancer research2014

Endothelial cell-secreted EGF induces epithelial to mesenchymal transition and endows head and neck cancer cells with stem-like phenotype.

Zhaocheng Zhang, Zhihong Dong, Isabel S Lauxen, Manoel Sant'Ana Filho, Jacques E Nör

Abstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

80 citing papers in PubMed, 131 citations in OpenAlex.

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20 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 2 countries.

Zhaocheng ZhangAuthors' Affiliations: Department of Restorative Sciences, Angiogenesis Research Laboratory, University of Michigan School of Dentistry; Department of Biomedical Engineering, University of Michigan College of Engineering; Department of Otolaryngology, University of Michigan School of Medicine, Ann Arbor, Michigan; and Department of Oral Pathology, School of Dentistry, Universidade Federal do Rio Grande do Sul; Porto Alegre, Rio Grande do Sul, Brazil.
Zhihong DongAuthors' Affiliations: Department of Restorative Sciences, Angiogenesis Research Laboratory, University of Michigan School of Dentistry; Department of Biomedical Engineering, University of Michigan College of Engineering; Department of Otolaryngology, University of Michigan School of Medicine, Ann Arbor, Michigan; and Department of Oral Pathology, School of Dentistry, Universidade Federal do Rio Grande do Sul; Porto Alegre, Rio Grande do Sul, Brazil.
Isabel S LauxenAuthors' Affiliations: Department of Restorative Sciences, Angiogenesis Research Laboratory, University of Michigan School of Dentistry; Department of Biomedical Engineering, University of Michigan College of Engineering; Department of Otolaryngology, University of Michigan School of Medicine, Ann Arbor, Michigan; and Department of Oral Pathology, School of Dentistry, Universidade Federal do Rio Grande do Sul; Porto Alegre, Rio Grande do Sul, Brazil.
Manoel Sant'Ana FilhoAuthors' Affiliations: Department of Restorative Sciences, Angiogenesis Research Laboratory, University of Michigan School of Dentistry; Department of Biomedical Engineering, University of Michigan College of Engineering; Department of Otolaryngology, University of Michigan School of Medicine, Ann Arbor, Michigan; and Department of Oral Pathology, School of Dentistry, Universidade Federal do Rio Grande do Sul; Porto Alegre, Rio Grande do Sul, Brazil.
Jacques E NörAuthors' Affiliations: Department of Restorative Sciences, Angiogenesis Research Laboratory, University of Michigan School of Dentistry; Department of Biomedical Engineering, University of Michigan College of Engineering; Department of Otolaryngology, University of Michigan School of Medicine, Ann Arbor, Michigan; and Department of Oral Pathology, School of Dentistry, Universidade Federal do Rio Grande do Sul; Porto Alegre, Rio Grande do Sul, BrazilAuthors' Affiliations: Department of Restorative Sciences, Angiogenesis Research Laboratory, University of Michigan School of Dentistry; Department of Biomedical Engineering, University of Michigan College of Engineering; Department of Otolaryngology, University of Michigan School of Medicine, Ann Arbor, Michigan; and Department of Oral Pathology, School of Dentistry, Universidade Federal do Rio Grande do Sul; Porto Alegre, Rio Grande do Sul, BrazilAuthors' Affiliations: Department of Restorative Sciences, Angiogenesis Research Laboratory, University of Michigan School of Dentistry; Department of Biomedical Engineering, University of Michigan College of Engineering; Department of Otolaryngology, University of Michigan School of Medicine, Ann Arbor, Michigan; and Department of Oral Pathology, School of Dentistry, Universidade Federal do Rio Grande do Sul; Porto Alegre, Rio Grande do Sul, Brazil jenor@umich.edu.
Universidade Federal do Rio Grande do Sul · BRUniversity of Michigan–Ann Arbor · US

Funding

Therapeutic Potential and Mechanism of Action of Potent Small Molecule InhibitorsP50CA097248 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WOLF, GREGORY T · 2002 to 2013
$25.3M
Salivary gland cancer stem cellsR01DE021139 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Jacques Eduardo Nor · 2011 to 2026
$5.8M
Therapeutic Inhibition of MDM2/Bcl-2 in Pre-clinical Models of Adenoid Cystic CarR01DE023220 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NOR, JACQUES EDUARDO · 2012 to 2015
$1.5M
Endothelial and head & neck cancer stem cell crosstalks and resistance to therapyR21DE019279 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NOR, JACQUES EDUARDO · 2008 to 2009
$419k
NCI NIH HHS P50 CA097248NCI NIH HHS P50-CA97248NIDCR NIH HHS R01 DE021139NIDCR NIH HHS R01 DE023220NIDCR NIH HHS R01-DE21139NIDCR NIH HHS R01-DE23220NIDCR NIH HHS R21 DE019279NIDCR NIH HHS R21-DE19279
6 · The paper itself

Abstract

Emerging evidence suggests that endothelial cell-secreted factors contribute to the pathobiology of squamous cell carcinoma (SCC) by enhancing invasive migration and resistance to anoikis. Here, we report that SCC cells within the perivascular niche have undergone epithelial to mesenchymal transition (EMT) in a primary human SCC of a patient that developed distant metastases. Endothelial cell-secreted EGF induced EMT of human SCC cells in vitro and also induced acquisition of a stem-like phenotype. In vivo, tumor xenografts vascularized with EGF-silenced endothelial cells exhibited a smaller fraction of cancer stem-like cells (ALDH(+)CD44(+)) and were less invasive than tumors vascularized with control endothelial cells. Collectively, these results demonstrated that endothelial cell-EGF induces EMT and acquisition of stem-like properties by head and neck tumor cells. On this basis, we suggest that vascular endothelial cells contribute to tumor dissemination by secreting factors that endow carcinoma cells with enhanced motility and stemness.

Indexed as

AgedAnimalsCarcinoma, Squamous CellCell CommunicationCell Growth ProcessesCell Line, TumorCell MovementEndothelial CellsEpidermal Growth FactorEpithelial-Mesenchymal TransitionHead and Neck NeoplasmsHeterograftsHumansMaleMiceMice, SCIDEpidermal Growth FactorPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID24686166
PMCPMC4028029
OpenAlexW2039721235

What OpenQuestion holds

Textmetadata
LicenceTDM
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.