Evidence map›Paper›PMID 37661833›Full record

ArticleThe EMBO journal2023

A mitochondrial EglN1-AMPKα axis drives breast cancer progression by enhancing metabolic adaptation to hypoxic stress.

Weiwei Jiang, Mengyao Zhang, Chuan Gao, Chaojun Yan, Ronghui Gao, Ziwei He, Xin Wei, Jingjing Xiong, Zilun Ruan, Qian Yang and 14 more

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
5.3field-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

15 citing papers in PubMed, 22 citations in OpenAlex.

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  8. Mitochondrial metabolism and cancer therapeutic innovation.Signal transduction and targeted therapy · 2025
    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

24 authors at 4 institutions in 1 country.

Weiwei Jiang *Department of Thyroid and Breast Surgery, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Mengyao Zhang *Department of Thyroid and Breast Surgery, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Chuan Gao *Department of Thyroid and Breast Surgery, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Chaojun YanDepartment of Thyroid and Breast Surgery, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.ORCID 0000-0002-2779-0642
Ronghui GaoDepartment of Thyroid and Breast Surgery, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Ziwei HeDepartment of Thyroid and Breast Surgery, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Xin WeiLife Sciences Institute, Zhejiang University, Hangzhou, China.ORCID 0000-0001-6635-5531
Jingjing XiongDepartment of Thyroid and Breast Surgery, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Zilun RuanFrontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan, China.ORCID 0000-0003-0677-8377
Qian YangDepartment of Thyroid and Breast Surgery, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Jinpeng LiDepartment of Thyroid and Breast Surgery, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Qifang LiDepartment of Thyroid and Breast Surgery, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Ziyi ZhongDepartment of Thyroid and Breast Surgery, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Mengna ZhangDepartment of Thyroid and Breast Surgery, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Qianqian YuanDepartment of Thyroid and Breast Surgery, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Hankun HuDepartment of Pharmacy, Zhongnan Hospital of Wuhan University, School of Pharmaceutical Sciences, Wuhan University, Wuhan, China.ORCID 0000-0001-5797-1770
Shuang WangMabnus Biological Technology Incorporation, Wuhan, China.
Ming-Ming HuFrontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan, China.
Cheguo CaiDepartment of Thyroid and Breast Surgery, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.ORCID 0000-0002-3712-1696
Gao-Song WuDepartment of Thyroid and Breast Surgery, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Chao JiangLife Sciences Institute, Zhejiang University, Hangzhou, China.
Ya-Lin ZhangState Key Laboratory for Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Fujian, China.
Chen-Song ZhangState Key Laboratory for Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Fujian, China.
Jing ZhangDepartment of Thyroid and Breast Surgery, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.ORCID 0000-0001-6438-9113
Wuhan University · CNXiamen University · CNZhejiang University · CNWuhan University of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria play essential roles in cancer cell adaptation to hypoxia, but the underlying mechanisms remain elusive. Through mitochondrial proteomic profiling, we here find that the prolyl hydroxylase EglN1 (PHD2) accumulates on mitochondria under hypoxia. EglN1 substrate-binding region in the β2β3 loop is responsible for its mitochondrial translocation and contributes to breast tumor growth. Furthermore, we identify AMP-activated protein kinase alpha (AMPKα) as an EglN1 substrate on mitochondria. The EglN1-AMPKα interaction is essential for their mutual mitochondrial translocation. After EglN1 prolyl-hydroxylates AMPKα under normoxia, they rapidly dissociate following prolyl-hydroxylation, leading to their immediate release from mitochondria. In contrast, hypoxia results in constant EglN1-AMPKα interaction and their accumulation on mitochondria, leading to the formation of a Ca

Indexed as

AMP-Activated Protein KinasesBreast NeoplasmsFemaleHumansHypoxiaHypoxia-Inducible Factor-Proline DioxygenasesMitochondriaProteomicsAMP-Activated Protein KinasesEGLN1 protein, humanHypoxia-Inducible Factor-Proline DioxygenasesAMPKαEglN1hypoxiametabolic homeostasismitochondrial translocation

Identifiers

PMID37661833
PMCPMC10577635
OpenAlexW4386407981

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.