Evidence map›Paper›PMID 27683113›Full record

ArticleOncotarget2016

ESM1 mediates NGFR-induced invasion and metastasis in murine oral squamous cell carcinoma.

Chen Chen, June Ho Shin, Joshua T Eggold, Man Ki Chung, Luhua H Zhang, Jeremy Lee, John B Sunwoo

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  11. Perineural Invasion in Head and Neck Cancer.Journal of dental research · 2018
    Review
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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 3 countries.

Chen ChenDivision of Head and Neck Surgery, Department of Otolaryngology, Stanford University School of Medicine, Stanford, CA 94305, USA.
June Ho ShinDivision of Head and Neck Surgery, Department of Otolaryngology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Joshua T EggoldStanford Cancer Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Man Ki ChungDivision of Head and Neck Surgery, Department of Otolaryngology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Luhua H ZhangDivision of Head and Neck Surgery, Department of Otolaryngology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Jeremy LeeDivision of Head and Neck Surgery, Department of Otolaryngology, Stanford University School of Medicine, Stanford, CA 94305, USA.
John B SunwooDivision of Head and Neck Surgery, Department of Otolaryngology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Stanford University · USSamsung Medical Center · KR

Funding

Identification of Cooperative Genetic Alterations in the Pathogenesis of Oral CancerU01DE025188 · NIDCR · STANFORD UNIVERSITY · PI GEVAERT, OLIVIER, KUO, CALVIN J · 2015 to 2018
$3.8M
NIDCR NIH HHS U01 DE025188
6 · The paper itself

Abstract

Oral squamous cell carcinoma (OSCC) is a highly invasive and metastatic malignancy. The nerve growth factor receptor (NGFR) has been observed to be expressed on a subset of cells in OSCC, and NGFR+ cells have greater tumor-initiating capacity in vivo. Further, inhibition of NGFR reduces tumor growth, indicating a functional role of this receptor; however, the mechanisms by which NGFR confers enhanced tumor formation are not known. Here, we used an established murine model of OSCC and gene expression array analysis to identify ESM1 as a downstream target gene of NGFR, critical for tumor invasion and metastasis. ESM1 encodes a protein called endocan, which has the property of regulating proliferation, differentiation, migration, and adhesion of different cell types. Incubation of NGFR+ murine OSCC cells with nerve growth factor resulted in increased expression of ESM1. Importantly, ESM1 overexpression conferred an enhanced migratory, invasive, and metastatic phenotype, similar to what has been correlated with NGFR expression. Conversely, shRNA knockdown of ESM1 in NGFR overexpressing OSCC cells abrogated the tumor growth kinetics and the invasive and metastatic properties associated with NGFR. Together, our data indicate that NGFR plays an important role in the pathogenesis and progression of OSCC via regulation of ESM1.

Indexed as

AnimalsCarcinoma, Squamous CellCell Line, TumorCell MovementFluorescent Antibody TechniqueGene Expression ProfilingGene Knockdown TechniquesHumansLung NeoplasmsMiceMouth NeoplasmsNeoplasm InvasivenessNerve Growth FactorProteoglycansReceptor, Nerve Growth FactorRNA Interferenceendothelial cell-specific molecule-1, mouseNerve Growth FactorProteoglycansReceptor, Nerve Growth FactorRNA, Small InterferingCD271endocanHNSCCmetastasisnerve growth factor receptor

Identifiers

PMID27683113
PMCPMC5342586
OpenAlexW2521178523

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.