Evidence map›Paper›PMID 28842347›Full record

ReviewFree radical biology & medicine2017

Extracellular superoxide dismutase and its role in cancer.

Brandon Griess, Eric Tom, Frederick Domann, Melissa Teoh-Fitzgerald

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Free radical biology & medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 2 pooled it
5.0field-weighted citation impact, top 4% 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

89 citing papers in PubMed, 2 syntheses or guidelines pooled it, 199 citations in OpenAlex.

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29 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Brandon GriessDepartment of Biochemistry and Molecular Biology, Buffett Cancer Center, College of Medicine, University of Nebraska Medical Center, Omaha, NE 68198, United States.
Eric TomDepartment of Biochemistry and Molecular Biology, Buffett Cancer Center, College of Medicine, University of Nebraska Medical Center, Omaha, NE 68198, United States.
Frederick DomannFree Radical and Radiation Biology Program, Radiation Oncology, University of Iowa, Iowa, IA 52242, United States.
Melissa Teoh-FitzgeraldDepartment of Biochemistry and Molecular Biology, Buffett Cancer Center, College of Medicine, University of Nebraska Medical Center, Omaha, NE 68198, United States. Electronic address: m.teohfitzgerald@unmc.edu.
University of Nebraska Medical Center · USUniversity of Iowa · US

Funding

CHEMICAL CARCINOGENESIS &CANCER BIOLOGYT32CA009476 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Jennifer D. Black · 1988 to 2026
$6.2M
Extracellular Redox Signaling in mammary tumor-fibroblast interactionsR01CA182086 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI TEOH, MELISSA LAI TEE · 2014 to 2018
$1.5M
Molecular Species Responsible for Tumor Supressive Effect of MnSODR01CA115438 · NCI · UNIVERSITY OF IOWA · PI DOMANN, FREDERICK E · 2007 to 2011
$1.2M
NCI NIH HHS R01 CA115438NCI NIH HHS R01 CA182086NCI NIH HHS T32 CA009476
6 · The paper itself

Abstract

Reactive oxygen species (ROS) are increasingly recognized as critical determinants of cellular signaling and a strict balance of ROS levels must be maintained to ensure proper cellular function and survival. Notably, ROS is increased in cancer cells. The superoxide dismutase family plays an essential physiological role in mitigating deleterious effects of ROS. Due to the compartmentalization of ROS signaling, EcSOD, the only superoxide dismutase in the extracellular space, has unique characteristics and functions in cellular signal transduction. In comparison to the other two intracellular SODs, EcSOD is a relatively new comer in terms of its tumor suppressive role in cancer and the mechanisms involved are less well understood. Nevertheless, the degree of differential expression of this extracellular antioxidant in cancer versus normal cells/tissues is more pronounced and prevalent than the other SODs. A significant association of low EcSOD expression with reduced cancer patient survival further suggests that loss of extracellular redox regulation promotes a conducive microenvironment that favors cancer progression. The vast array of mechanisms reported in mediating deregulation of EcSOD expression, function, and cellular distribution also supports that loss of this extracellular antioxidant provides a selective advantage to cancer cells. Moreover, overexpression of EcSOD inhibits tumor growth and metastasis, indicating a role as a tumor suppressor. This review focuses on the current understanding of the mechanisms of deregulation and tumor suppressive function of EcSOD in cancer.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAntioxidantsExtracellular SpaceHumansNeoplasmsOxidation-ReductionOxidative StressReactive Oxygen SpeciesSignal TransductionSuperoxide DismutaseSurvival AnalysisTumor MicroenvironmentAntioxidantsReactive Oxygen SpeciesSuperoxide DismutaseCancerEcSODEpigeneticHeparin binding domainLoss of heterozygosityMetastasismicroRNA-21Oxidative tumor microenvironmentReactive oxygen speciesRecurrenceRelapse free survivalSingle nucleotide polymorphismSOD3Tumor suppressor

Identifiers

PMID28842347
PMCPMC5685559
OpenAlexW2746781208

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.