Evidence map›Paper›PMID 20489156›Full record

ArticleThe American journal of pathology2010

Early growth response-1 induces and enhances vascular endothelial growth factor-A expression in lung cancer cells.

Hiroaki Shimoyamada, Takuya Yazawa, Hanako Sato, Koji Okudela, Jun Ishii, Masashi Sakaeda, Korehito Kashiwagi, Takehisa Suzuki, Hideaki Mitsui, Tetsukan Woo and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 59 citations in OpenAlex.

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  11. Friend or foe, the role of EGR-1 in cancer.Medical oncology (Northwood, London, England) · 2019
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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

16 authors at 4 institutions in 1 country.

Hiroaki ShimoyamadaDepartment of Pathology, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, Kanagawa 236-0004, Japan.
Takuya Yazawa
Hanako Sato
Koji Okudela
Jun Ishii
Masashi Sakaeda
Korehito Kashiwagi
Takehisa Suzuki
Hideaki Mitsui
Tetsukan Woo
Michihiko Tajiri
Takahiro Ohmori
Takashi Ogura
Munetaka Masuda
Hisashi Oshiro
Hitoshi Kitamura
Yokohama City University · JPKanagawa Cardiovascular and Respiratory Center · JPSt. Marianna University School of Medicine · JPYokohama City University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular endothelial growth factor-A (VEGF-A) is crucial for angiogenesis, vascular permeability, and metastasis during tumor development. We demonstrate here that early growth response-1 (EGR-1), which is induced by the extracellular signal-regulated kinase (ERK) pathway activation, activates VEGF-A in lung cancer cells. Increased EGR-1 expression was found in adenocarcinoma cells carrying mutant K-RAS or EGFR genes. Hypoxic culture, siRNA experiment, luciferase assays, chromatin immunoprecipitation, electrophoretic mobility shift assays, and quantitative RT-PCR using EGR-1-inducible lung cancer cells demonstrated that EGR-1 binds to the proximal region of the VEGF-A promoter, activates VEGF-A expression, and enhances hypoxia inducible factor 1alpha (HIF-1alpha)-mediated VEGF-A expression. The EGR-1 modulator, NAB-2, was rapidly induced by increased levels of EGR-1. Pathology samples of human lung adenocarcinomas revealed correlations between EGR-1/HIF-1alpha and VEGF-A expressions and relative elevation of EGR-1 and VEGF-A expression in mutant K-RAS- or EGFR-carrying adenocarcinomas. Both EGR-1 and VEGF-A expression increased as tumors dedifferentiated, whereas HIF-1alpha expression did not. Although weak correlation was found between EGR-1 and NAB-2 expressions on the whole, NAB-2 expression decreased as tumors dedifferentiated, and inhibition of DNA methyltransferase/histone deacetylase increased NAB-2 expression in lung cancer cells despite no epigenetic alteration in the NAB-2 promoter. These findings suggest that EGR-1 plays important roles on VEGF-A expression in lung cancer cells, and epigenetic silencing of transactivator(s) associated with NAB-2 expression might also contribute to upregulate VEGF-A expression.

Indexed as

AdenocarcinomaAnimalsAzacitidineCell Line, TumorDecitabineEarly Growth Response Protein 1Enzyme InhibitorsExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, NeoplasticGenes, rasHumansHypoxia-Inducible Factor 1, alpha SubunitLung NeoplasmsPromoter Regions, GeneticRepressor ProteinsRNA InterferenceAzacitidineDecitabineEarly Growth Response Protein 1EGR1 protein, humanEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesHypoxia-Inducible Factor 1, alpha SubunitNAB2 protein, humanRepressor ProteinsVascular Endothelial Growth Factor A

Identifiers

PMID20489156
PMCPMC2893652
OpenAlexW1975357118

What OpenQuestion holds

Textmetadata
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.