Evidence map›Paper›PMID 26492917›Full record

ArticleThe EMBO journal2015

EglN2 associates with the NRF1-PGC1α complex and controls mitochondrial function in breast cancer.

Jing Zhang, Chengyang Wang, Xi Chen, Mamoru Takada, Cheng Fan, Xingnan Zheng, Haitao Wen, Yong Liu, Chenguang Wang, Richard G Pestell and 4 more

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

61 citing papers in PubMed, 71 citations in OpenAlex.

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1 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

14 authors at 8 institutions in 2 countries.

Jing ZhangLineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC, USA.
Chengyang WangDepartment of Bioinformatics, School of Life Science and Technology, Tongji University, Shanghai, China.
Xi ChenDepartment of Molecular and Cellular Biology, The Lester and Sue Smith Breast Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX, USA.
Mamoru TakadaLineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC, USA.
Cheng FanLineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC, USA.
Xingnan ZhengLineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC, USA.
Haitao WenLineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC, USA Department of Surgery, University of North Carolina, Chapel Hill, NC, USA.
Yong LiuLineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC, USA.
Chenguang WangProgram of Radiation Protection and Drug Discovery, Institute of Radiation Medicine, Chinese Academy of Medical Sciences, Peking Union Medical College, Tianjin, China.
Richard G PestellDepartment of Cancer Biology and Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA.
Katherine M AirdGene Expression and Regulation Program, The Wistar Institute, Philadelphia, PA, USA.
William G KaelinDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA Howard Hughes Medical Institute, Chevy Chase, MD, USA.
Xiaole Shirley LiuDepartment of Biostatistics and Computational Biology, Dana-Farber Cancer Institute and Harvard School of Public Health, Boston, MA, USA.
Qing ZhangLineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC, USA Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC, USA qing_zhang@med.unc.edu.
University of North Carolina at Chapel Hill · USUNC Lineberger Comprehensive Cancer CenterTongji University · CNBaylor College of Medicine · USDana-Farber Cancer Institute · USHarvard University · USThe Wistar Institute · USThomas Jefferson University · US

Funding

X-Ray Crystallography and Macromolecular CharacterizationP30CA056036 · NCI · THOMAS JEFFERSON UNIVERSITY · PI DANIEL P SILVER · 1995 to 2026
$94.8M
Tissue Procurement & PathologyP50CA058223 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KATHERINE A. HOADLEY · 1992 to 2026
$59.3M
The von Hippel-Lindau Tumor Suppressor Protein:Roles in Cancer and Oxygen SensingR01CA068490 · NCI · DANA-FARBER CANCER INSTITUTE · PI KAELIN, WILLIAM G. · 1996 to 2015
$4.8M
Role of the EglN2 Target FOXO3a in Breast CancerR00CA160351 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ZHANG, QING · 2013 to 2015
$725k
Role of the EglN2 Target FOXO3a in Breast CancerK99CA160351 · NCI · DANA-FARBER CANCER INST · PI ZHANG, QING · 2011 to 2012
$270k
Howard Hughes Medical InstituteNCI NIH HHS 2R01CA68490NCI NIH HHS K99 CA160351NCI NIH HHS K99/R00 CA160351NCI NIH HHS P30 CA056036NCI NIH HHS P50 CA058223NCI NIH HHS R00 CA160351NCI NIH HHS R01 CA068490
6 · The paper itself

Abstract

The EglN2/PHD1 prolyl hydroxylase is an important oxygen sensor contributing to breast tumorigenesis. Emerging studies suggest that there is functional cross talk between oxygen sensing and mitochondrial function, both of which play an essential role for sustained tumor growth. However, the potential link between EglN2 and mitochondrial function remains largely undefined. Here, we show that EglN2 depletion decreases mitochondrial respiration in breast cancer under normoxia and hypoxia, which correlates with decreased mitochondrial DNA in a HIF1/2α-independent manner. Integrative analyses of gene expression profile and genomewide binding of EglN2 under hypoxic conditions reveal nuclear respiratory factor 1 (NRF1) motif enrichment in EglN2-activated genes, suggesting NRF1 as an EglN2 binding partner. Mechanistically, by forming an activator complex with PGC1α and NRF1 on chromatin, EglN2 promotes the transcription of ferridoxin reductase (FDXR) and maintains mitochondrial function. In addition, FDXR, as one of effectors for EglN2, contributes to breast tumorigenesis in vitro and in vivo. Our findings suggest that EglN2 regulates mitochondrial function in ERα-positive breast cancer.

Indexed as

Breast NeoplasmsCell Line, TumorFemaleHumansHypoxia-Inducible Factor-Proline DioxygenasesMitochondriaNF-E2-Related Factor 1Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaProtein BindingTranscription FactorsEGLN2 protein, humanHypoxia-Inducible Factor-Proline DioxygenasesNF-E2-Related Factor 1Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanTranscription FactorsEglN2hypoxiamitochondriaNRF1tumorigenesis

Identifiers

PMID26492917
PMCPMC4687683
OpenAlexW2123658031

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.