Evidence map›Paper›PMID 19435811›Full record

ArticleMolecular cancer research : MCR2009

A key role for early growth response-1 and nuclear factor-kappaB in mediating and maintaining GRO/CXCR2 proliferative signaling in esophageal cancer.

Bo Wang, Levon M Khachigian, Luke Esau, Michael J Birrer, Xiaohang Zhao, M Iqbal Parker, Denver T Hendricks

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.9field-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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
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  8. International journal of molecular sciences · 2022
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  19. Clinical significance of serum expression of GROβ in hepatocellular carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    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

7 authors at 5 institutions in 3 countries.

Bo WangDivision of Medical Biochemistry, Institute of Infectious Disease and Molecular Medicine, Faculty of Health Sciences, University of Cape Town, Anzio Road, Observatory, Cape Town 7925, South Africa.
Levon M Khachigian
Luke Esau
Michael J Birrer
Xiaohang Zhao
M Iqbal Parker
Denver T Hendricks
Chinese Academy of Medical Sciences & Peking Union Medical College · CNNational Cancer Institute · USCenter for Cancer Research · USMolecular Oncology (United States) · USUNSW Sydney · AU

Funding

USE OF TRANSCRIPTIONAL FACTORS AS TARGETS AND AGENTS IN CARCINOGENESISZ01SC000165 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI BIRRER, MICHAEL · 1996 to 2008
$974k
NDRG1 in squamous cell oesophageal cancerR01CA112020 · NCI · UNIVERSITY OF CAPE TOWN · PI HENDRICKS, DENVER T · 2004 to 2008
$261k
The Use of Transcriptional Factors as Targets and Agents in CarcinogenesisZIASC000165 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI BIRRER, MICHAEL · 2009 to 2009
$187k
THE MOLECULAR MECHANISMS OF ONCOGENE ACTIONZ01SC000164 · SC · CLINICAL SCIENCES · PI BIRRER, MICHAEL · 1996 to 2006
–
Intramural NIH HHS Z01 SC000164Intramural NIH HHS Z01 SC000165NCI NIH HHS 5R01 CA 112020NCI NIH HHS R01 CA112020
6 · The paper itself

Abstract

Although early growth response-1 (EGR-1) has been shown as a key transcription factor in controlling cell growth, proliferation, differentiation, and angiogenesis, its role in the development of esophageal cancer is poorly understood despite the high frequency of this disease in many parts of the world. Here, immunohistochemistry showed that EGR-1 is overexpressed in 80% of esophageal tumor tissues examined. Furthermore, EGR-1 is constitutively expressed in all esophageal cancer cell lines analyzed. Esophageal squamous carcinoma WHCO1 cells stably transfected with EGR-1 short hairpin RNA displayed a 55% reduction in EGR-1 protein levels, 50% reduction in cell proliferation, a 50% reduction in cyclin-dependent kinase 4 levels, and a 2-fold induction in p27(Kip1) levels associated with a G(2)-M cell cycle arrest. EGR-1 knockdown also caused a marked induction in IkappaBalpha expression, an effect also observed in GRObeta RNA interference-expressing WHCO1 cells, because EGR-1 lies downstream of GRO/CXCR2 signaling. Furthermore, p65 mRNA levels were also reduced in cells treated with either short hairpin RNA EGR-1 or small interfering RNA EGR-1. Immunohistochemical analysis indicated that p65 is elevated in 78% (n = 61) of esophageal tumor sections analyzed. Moreover, nuclear factor-kappaB inhibition with either sodium salicylate or p65 RNA interference led to a significant reduction in GROalpha and GRObeta expression. These results indicate that EGR-1 and nuclear factor-kappaB mediate GRO/CXCR2 proliferative signaling in esophageal cancer and may represent potential target molecules for therapeutic intervention.

Indexed as

Signal TransductionBlotting, WesternCell CycleCell Cycle ProteinsCell Line, TumorCell ProliferationChemokine CXCL1Chemokine CXCL2Early Growth Response Protein 1Esophageal NeoplasmsFluorescent Antibody TechniqueGene Expression Regulation, NeoplasticHumansImmunohistochemistryNF-kappa BReceptors, Interleukin-8BCell Cycle ProteinsChemokine CXCL1Chemokine CXCL2CXCL2 protein, humanEarly Growth Response Protein 1NF-kappa BReceptors, Interleukin-8BRNA, Small InterferingSodium SalicylateTranscription Factor RelA

Identifiers

PMID19435811
PMCPMC6944287
OpenAlexW2104025882

What OpenQuestion holds

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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.