Evidence map›Paper›PMID 26422659›Full record

ArticleAntioxidants & redox signaling2015

Mitochondrial Dysfunction Due to Lack of Manganese Superoxide Dismutase Promotes Hepatocarcinogenesis.

Anja Konzack, Mirza Jakupovic, Kateryna Kubaichuk, Agnes Görlach, Frank Dombrowski, Ilkka Miinalainen, Raija Sormunen, Thomas Kietzmann

Open access · hybridAbstract read
In one paragraph

Article in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 29 citations in OpenAlex.

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  8. Impaired Mitochondrial Fatty Acid Synthesis Leads to Neurodegeneration in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
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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

8 authors at 4 institutions in 2 countries.

Anja Konzack1 Faculty of Biochemistry and Molecular Medicine, and Biocenter Oulu, University of Oulu , Oulu, Finland .
Mirza Jakupovic2 Department of Chemistry, University of Kaiserslautern , Kaiserslautern, Germany .
Kateryna Kubaichuk1 Faculty of Biochemistry and Molecular Medicine, and Biocenter Oulu, University of Oulu , Oulu, Finland .
Agnes Görlach3 Experimental and Molecular Pediatric Cardiology, German Heart Center Munich, Technical University Munich , Munich, Germany .
Frank Dombrowski4 Institute of Pathology, University of Greifswald , Greifswald, Germany .
Ilkka Miinalainen5 Biocenter Oulu Electron Microscopy Core Facility, University of Oulu , Oulu, Finland .
Raija Sormunen5 Biocenter Oulu Electron Microscopy Core Facility, University of Oulu , Oulu, Finland .
Thomas Kietzmann1 Faculty of Biochemistry and Molecular Medicine, and Biocenter Oulu, University of Oulu , Oulu, Finland .
University of Oulu · FIDeutsches Herzzentrum München · DEUniversitätsmedizin Greifswald · DEUniversity of Kaiserslautern · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsOne of the cancer hallmarks is mitochondrial dysfunction associated with oxidative stress. Among the first line of defense against oxidative stress is the dismutation of superoxide radicals, which in the mitochondria is carried out by manganese superoxide dismutase (MnSOD). Accordingly, carcinogenesis would be associated with a dysregulation in MnSOD expression. However, the association studies available so far are conflicting, and no direct proof concerning the role of MnSOD as a tumor promoter or suppressor has been provided. Therefore, we investigated the role of MnSOD in carcinogenesis by studying the effect of MnSOD deficiency in cells and in the livers of mice.

resultsWe found that loss of MnSOD in hepatoma cells contributed to their conversion toward a more malignant phenotype, affecting all cellular properties generally associated with metabolic transformation and tumorigenesis. In vivo, hepatocyte-specific MnSOD-deficient mice showed changed organ architecture, increased expression of tumor markers, and a faster response to carcinogenesis. Moreover, deficiency of MnSOD in both the in vitro and in vivo model reduced β-catenin and hypoxia-inducible factor-1α levels. INNOVATION: The present study shows for the first time the important correlation between MnSOD presence and the regulation of two major pathways involved in carcinogenesis, the Wnt/β-catenin and hypoxia signaling pathway.

conclusionOur study points toward a tumor suppressive role of MnSOD in liver, where the Wnt/β-catenin and hypoxia pathway may be crucial elements.

Indexed as

AnimalsCarcinoma, HepatocellularCell HypoxiaCell ProliferationCell ShapeCell Transformation, NeoplasticDiethylnitrosamineHepatocytesHep G2 CellsHumansHypoxia-Inducible Factor 1, alpha SubunitLiver Neoplasms, ExperimentalMaleMice, KnockoutMitochondriaReactive Oxygen Species3-nitrotyrosineDiethylnitrosamineHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitReactive Oxygen SpeciesSuperoxide DismutaseSuperoxide Dismutase 2Tyrosine

Identifiers

PMID26422659
PMCPMC4657515
OpenAlexW2112403518

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.