Evidence map›Paper›PMID 16262603›Full record

ArticleThe Biochemical journal2006

Induction of spermidine/spermine N1-acetyltransferase (SSAT) by aspirin in Caco-2 colon cancer cells.

Naveen Babbar, Eugene W Gerner, Robert A Casero

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
3.3field-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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

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  10. Acetylsalicylic Acid-Primus Inter Pares in Pharmacology.Molecules (Basel, Switzerland) · 2022
    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

3 authors at 2 institutions in 1 country.

Naveen BabbarThe Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. nbabbar1@jhmi.edu
Eugene W Gerner
Robert A Casero
Johns Hopkins University · USUniversity of Arizona · US

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Dan Theodorescu · 1985 to 2026
$110.2M
SPORE in Gastrointestinal CancerP50CA095060 · NCI · UNIVERSITY OF ARIZONA · PI GERNER, EUGENE W · 2002 to 2012
$25.3M
RESISTANCE TO BILE ACID INDUCED APOPTOSISP01CA072008 · NCI · UNIVERSITY OF ARIZONA · PI GERNER, EUGENE W · 1997 to 2005
$6.9M
Spermine N1-Acetylase Induction in Lung CancersR01CA051085 · NCI · JOHNS HOPKINS UNIVERSITY · PI CASERO, ROBERT A. · 1990 to 2013
$4.7M
The Role of Polyamine Oxidase in Antitumor Drug ResponseR01CA098454 · NCI · JOHNS HOPKINS UNIVERSITY · PI CASERO, ROBERT A. · 2003 to 2013
$2.9M
NCI NIH HHS CA 23074NCI NIH HHS CA 51085NCI NIH HHS CA 72008NCI NIH HHS CA 95060NCI NIH HHS CA 98454NCI NIH HHS P01 CA072008NCI NIH HHS P30 CA023074NCI NIH HHS P50 CA095060NCI NIH HHS R01 CA051085NCI NIH HHS R01 CA098454
6 · The paper itself

Abstract

Epidemiological, experimental and clinical results suggest that aspirin and other NSAIDs (non-steroidal anti-inflammatory drugs) inhibit the development of colon cancer. It has been shown that the NSAID sulindac induces apoptosis and suppresses carcinogenesis, in part, by a mechanism leading to the transcriptional activation of the gene encoding SSAT (spermidine/spermine N1-acetyltransferase), a rate-limiting enzyme in polyamine catabolism. In the present study, we show that a variety of NSAIDs, including aspirin, sulindac, ibuprofen and indomethacin, can induce SSAT gene expression in Caco-2 cells. Aspirin, at physiological concentrations, can induce SSAT mRNA via transcriptional initiation mechanisms. This induction leads to increased SSAT protein levels and enzyme activity. Promoter deletion analysis of the 5' SSAT promoter-flanking region led to the identification of two NF-kappaB (nuclear factor kappaB) response elements. Electrophoretic mobility-shift assays showed binding of NF-kappaB complexes at these sequences after aspirin treatment. Aspirin treatment led to the activation of NF-kappaB signalling and increased binding at these NF-kappaB sites in the SSAT promoter, hence providing a potential mechanism for the induction of SSAT by aspirin in these cells. Aspirin-induced SSAT ultimately leads to a decrease in cellular polyamine content, which has been associated with decreased carcinogenesis. These results suggest that activation of SSAT by aspirin and different NSAIDs may be a common property of NSAIDs that plays an important role in their chemopreventive actions in colorectal cancer.

Indexed as

AcetyltransferasesAnti-Inflammatory Agents, Non-SteroidalAspirinCaco-2 CellsColonic NeoplasmsDiamine N-AcetyltransferaseDose-Response Relationship, DrugEnzyme InductionHumansNF-kappa BPeroxisome Proliferator-Activated ReceptorsPromoter Regions, GeneticProtein BindingResponse ElementsAcetyltransferasesAnti-Inflammatory Agents, Non-SteroidalAspirinDiamine N-AcetyltransferaseNF-kappa BPeroxisome Proliferator-Activated Receptors

Identifiers

PMID16262603
PMCPMC1386030
OpenAlexW2038580538

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.