Evidence map›Paper›PMID 31591207›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

SOD2 acetylation on lysine 68 promotes stem cell reprogramming in breast cancer.

Chenxia He, Jeanne M Danes, Peter C Hart, Yueming Zhu, Yunping Huang, Andre Luelsdorf de Abreu, Joseph O'Brien, Angela J Mathison, Binwu Tang, Jonna M Frasor and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

47 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
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  6. Deacetylation of SOD3 by sirtuins restores furin cleavage.Redox biochemistry and chemistry · 2025
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 5 institutions in 1 country.

Chenxia HeDepartment of Medicine, Division of Endocrinology, Medical College of Wisconsin, Milwaukee, WI 53226.
Jeanne M DanesDepartment of Medicine, Division of Endocrinology, Medical College of Wisconsin, Milwaukee, WI 53226.
Peter C HartDepartment of Pathology, University of Illinois at Chicago, Chicago, IL 60612.
Yueming ZhuDepartment of Radiation Oncology, Northwestern University, Chicago, IL 60657.
Yunping HuangDepartment of Medicine, Division of Endocrinology, Medical College of Wisconsin, Milwaukee, WI 53226.
Andre Luelsdorf de AbreuDepartment of Pathology, University of Illinois at Chicago, Chicago, IL 60612.
Joseph O'BrienDepartment of Radiation Oncology, Northwestern University, Chicago, IL 60657.
Angela J MathisonGenomic Sciences and Precision Medicine Center, Medical College of Wisconsin, Milwaukee, WI 53226.
Binwu TangCenter for Cancer Research, National Cancer Institute, Bethesda, MD 20892.
Jonna M FrasorDepartment of Physiology and Biophysics, University of Illinois at Chicago, Chicago, IL 60612.
Lalage M WakefieldCenter for Cancer Research, National Cancer Institute, Bethesda, MD 20892.
Douglas GaniniFree Radical Metabolism Group, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709.
Erich StauderDepartment of Biophysics, Medical College of Wisconsin, Milwaukee, WI 53226.
Jacek ZielonkaDepartment of Biophysics, Medical College of Wisconsin, Milwaukee, WI 53226.
Benjamin N GantnerDepartment of Medicine, Division of Endocrinology, Medical College of Wisconsin, Milwaukee, WI 53226.
Raul A UrrutiaGenomic Sciences and Precision Medicine Center, Medical College of Wisconsin, Milwaukee, WI 53226.
David GiusDepartment of Radiation Oncology, Northwestern University, Chicago, IL 60657.
Marcelo G BoniniDepartment of Medicine, Division of Endocrinology, Medical College of Wisconsin, Milwaukee, WI 53226; mbonini@mcw.edu.
Medical College of Wisconsin · USNorthwestern University · USUniversity of Illinois Chicago · USNational Cancer Institute · USNational Institute of Environmental Health Sciences · US

Funding

TRANSGENIC COREP30AG013319 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI JAMES FLOYD NELSON · 1995 to 2026
$30.6M
ZINC FINGER GENES AND PANCREATIC CELL GROWTHR01DK052913 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI LOMBERK, GWEN, URRUTIA, RAUL A. · 1998 to 2023
$7.0M
Estrogen Receptor and NFkB Crosstalk in Breast CancerR01CA200669 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI Jonathan L. Coloff · 2016 to 2026
$4.8M
Loss of mtSIRT3, Decreased MnSOD Activity, and IR Induced Genomic InstabilityR01CA152601 · NCI · VANDERBILT UNIVERSITY · PI BONINI, MARCELO G. · 2010 to 2019
$3.5M
New Strategies for Treating Septic Vasculopathy Inflammation and ThrombosisR01HL125356 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI BONINI, MARCELO G., DU, XIAOPING · 2014 to 2018
$3.4M
Macrophage Redox State in Sterilizing and Injurious InflammationR01AI131267 · NIAID · UNIVERSITY OF ILLINOIS AT CHICAGO · PI BONINI, MARCELO G. · 2017 to 2021
$2.1M
MnSOD-K68-Ac reprograms a lineage plasticity switch / stemness in ER+ breast malignancies.R01CA253678 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI GIUS, DAVID · 2021 to 2025
$2.1M
Dys-regulation of the MnSOD-Ac-ROS-HIF2a axis promotes IR / Cisplatin resistance phenotypeR01CA214025 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI GIUS, DAVID · 2017 to 2021
$2.0M
MNSOD ACETYLATION PROMOTES CANCER STEM CELL PHENOTYPES IN BREAST CANCERR01CA216882 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BONINI, MARCELO G. · 2018 to 2022
$1.9M
ROS and HIFa as molecular targets for chemoprevention in Sirt3 -/- breast cancersR01CA168292 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI GIUS, DAVID · 2012 to 2016
$1.9M
Environmental Arsenic in the Subtype Specification of Breast CancerR01ES028149 · NIEHS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BONINI, MARCELO G. · 2018 to 2022
$1.8M
SIRT3 is a Mitochondrial Tumor Suppressor in ER/PR Positive Mammary TumorsR01CA152799 · NCI · VANDERBILT UNIVERSITY · PI GIUS, DAVID · 2011 to 2015
$1.6M
NCI NIH HHS R01 CA152601NCI NIH HHS R01 CA152799NCI NIH HHS R01 CA168292NCI NIH HHS R01 CA200669NCI NIH HHS R01 CA214025NCI NIH HHS R01 CA216882NCI NIH HHS R01 CA253678NHLBI NIH HHS R01 HL125356NIAID NIH HHS R01 AI131267NIA NIH HHS P30 AG013319NIDDK NIH HHS R01 DK052913NIEHS NIH HHS R01 ES028149
6 · The paper itself

Abstract

Mitochondrial superoxide dismutase (SOD2) suppresses tumor initiation but promotes invasion and dissemination of tumor cells at later stages of the disease. The mechanism of this functional switch remains poorly defined. Our results indicate that as SOD2 expression increases acetylation of lysine 68 ensues. Acetylated SOD2 promotes hypoxic signaling via increased mitochondrial reactive oxygen species (mtROS). mtROS, in turn, stabilize hypoxia-induced factor 2α (HIF2α), a transcription factor upstream of "stemness" genes such as Oct4, Sox2, and Nanog. In this sense, our findings indicate that SOD2

Indexed as

AcetylationAnimalsBasic Helix-Loop-Helix ProteinsBreast NeoplasmsCell Self RenewalCellular ReprogrammingDisease ProgressionEndothelial PAS Domain-Containing Protein 1FemaleHeterograftsHumansHydrogen PeroxideMCF-7 CellsMiceMice, Inbred NODMice, SCIDBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1Hydrogen PeroxideNeoplasm ProteinsRecombinant ProteinsSuperoxide DismutaseSuperoxide Dismutase 2acetylationbreast cancerMnSODSOD2stem cells

Identifiers

PMID31591207
PMCPMC6876149
OpenAlexW2980111553

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.