Evidence map›Paper›PMID 28819251›Full record

ArticleNature communications2017

G9a regulates breast cancer growth by modulating iron homeostasis through the repression of ferroxidase hephaestin.

Ya-Fang Wang, Jie Zhang, Yi Su, Yan-Yan Shen, Dong-Xian Jiang, Ying-Yong Hou, Mei-Yu Geng, Jian Ding, Yi Chen

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.5field-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

55 citing papers in PubMed, 123 citations in OpenAlex.

  1. Review
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  9. Transmetalation in Cancer Pharmacology.International journal of molecular sciences · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Discovery of the First-in-Class G9a/GLP PROTAC Degrader.Journal of medicinal chemistry · 2024
    Article
  15. Discovery of the First-in-class G9a/GLP PROTAC Degrader.bioRxiv : the preprint server for biology · 2024
    Article
  16. Article
  17. Article
  18. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 1 country.

Ya-Fang WangDivision of Anti-Tumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Jie ZhangKey Laboratory of Systems Biology, CAS Center for Excellence in Molecular Cell Science, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
Yi SuDivision of Anti-Tumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Yan-Yan ShenDivision of Anti-Tumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Dong-Xian JiangDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Ying-Yong HouDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Mei-Yu GengDivision of Anti-Tumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China. mygeng@simm.ac.cn.
Jian DingDivision of Anti-Tumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China. jding@simm.ac.cn.
Yi ChenDivision of Anti-Tumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China. ychen@simm.ac.cn.
Chinese Academy of Sciences · CNShanghai Institute of Materia Medica · CNFudan University · CNShanghai Institutes for Biological Sciences · CNZhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G9a, a H3K9 methyltransferase, shows elevated expression in many types of human cancers, particularly breast cancer. However, the tumorigenic mechanism of G9a is still far from clear. Here we report that G9a exerts its oncogenic function in breast cancer by repressing hephaestin and destruction cellular iron homeostasis. In the case of pharmacological inhibition or short hairpin RNA interference-mediated suppression of G9a, the expression and activity of hephaestin increases, leading to the observed decrease of intracellular labile iron content and the disturbance of breast cancer cell growth in vitro and in vivo. We also provide evidence that G9a interacts with HDAC1 and YY1 to form a multi-molecular complex that contributes to hephaestin silencing. Furthermore, high G9a expression and low hephaestin expression correlate with poor survival of breast cancer are investigated. All these suggest a G9a-dependent epigenetic program in the control of iron homeostasis and tumor growth in breast cancer.G9a is a histone methyltransferase highly expressed in several cancers including breast cancer. Here the authors propose a mechanism through which G9a promotes breast cancer by regulating iron metabolism through the repression of ferroxidase hephaestin.

Indexed as

Gene Expression Regulation, NeoplasticBreast NeoplasmsCell Line, TumorCell ProliferationHistocompatibility AntigensHistone-Lysine N-MethyltransferaseHomeostasisHumansIronMembrane ProteinsReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionEHMT2 protein, humanHEPH protein, humanHistocompatibility AntigensHistone-Lysine N-MethyltransferaseIronMembrane Proteins

Identifiers

PMID28819251
PMCPMC5561105
OpenAlexW2743506403

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.