Evidence map›Paper›PMID 19401523›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2009

Nonsteroidal anti-inflammatory drug-activated gene-1 expression inhibits urethane-induced pulmonary tumorigenesis in transgenic mice.

Maria Cekanova, Seong-Ho Lee, Robert L Donnell, Mugdha Sukhthankar, Thomas E Eling, Susan M Fischer, Seung Joon Baek

Open access · bronzeAbstract read
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 73 citations in OpenAlex.

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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 3 institutions in 1 country.

Maria CekanovaDepartment of Pathobiology, College of Veterinary Medicine, The University of Tennessee, Knoxville, TN 37996, USA.
Seong-Ho Lee
Robert L Donnell
Mugdha Sukhthankar
Thomas E Eling
Susan M Fischer
Seung Joon Baek
National Institute of Environmental Health Sciences · USThe University of Texas MD Anderson Cancer Center · USUniversity of Tennessee at Knoxville · US

Funding

Anti-carcinogenic Activity Of Cox inhibitors and NAG-1ZIAES010016 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI ELING, THOMAS · 2009 to 2013
$8.3M
Role Of Lipids In Colon, Breast, And Other CancersZIAES050144 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI ELING, THOMAS · 2009 to 2012
$1.8M
PPAR-gamma ligands in colorectal cancerR01CA108975 · NCI · UNIVERSITY OF TENNESSEE KNOXVILLE · PI BAEK, SEUNG JOON · 2006 to 2010
$1.0M
Intramural NIH HHSNCI NIH HHS R01 CA 108975NCI NIH HHS R01 CA108975
6 · The paper itself

Abstract

The expression of nonsteroidal anti-inflammatory drug-activated gene-1 (NAG-1) inhibits gastrointestinal tumorigenesis in NAG-1 transgenic mice (C57/BL6 background). In the present study, we investigated whether the NAG-1 protein would alter urethane-induced pulmonary lesions in NAG-1 transgenic mice on an FVB background (NAG-1(Tg+/FVB)). NAG-1(Tg+/FVB) mice had both decreased number and size of urethane-induced tumors, compared with control littermates (NAG-1(Tg+/FVB) = 16 +/- 4 per mouse versus control = 20 +/- 7 per mouse, P < 0.05). Urethane-induced pulmonary adenomas and adenocarcinomas were observed in control mice; however, only pulmonary adenomas were observed in NAG-1(Tg+/FVB) mice. Urethane-induced tumors from control littermates and NAG-1(Tg+/FVB) mice highly expressed proteins in the arachidonic acid pathway (cyclooxygenases 1/2, prostaglandin E synthase, and prostaglandin E(2) receptor) and highly activated several kinases (phospho-Raf-1 and phosphorylated extracellular signal-regulated kinase 1/2). However, only urethane-induced p38 mitogen-activated protein kinase (MAPK) phosphorylation was decreased in NAG-1(Tg+/FVB) mice. Furthermore, significantly increased apoptosis in tumors of NAG-1(Tg+/FVB) mice compared with control mice was observed as assessed by caspase-3/7 activity. In addition, fewer inflammatory cells were observed in the lung tissue isolated from urethane-treated NAG-1(Tg+/FVB) mice compared with control mice. These results paralleled in vitro assays using human A549 pulmonary carcinoma cells. Less phosphorylated p38 MAPK was observed in cells overexpressing NAG-1 compared with control cells. Overall, our study revealed for the first time that the NAG-1 protein inhibits urethane-induced tumor formation, probably mediated by the p38 MAPK pathway, and is a possible new target for lung cancer chemoprevention.

Indexed as

AnimalsApoptosisBlotting, WesternCarcinogensCell Line, TumorGrowth Differentiation Factor 15HumansImmunohistochemistryIn Situ Nick-End LabelingLung NeoplasmsMiceMice, Transgenicp38 Mitogen-Activated Protein KinasesReverse Transcriptase Polymerase Chain ReactionSignal TransductionUrethaneCarcinogensGrowth Differentiation Factor 15p38 Mitogen-Activated Protein KinasesUrethane

Identifiers

PMID19401523
PMCPMC2697576
OpenAlexW2162856680

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.