Evidence map›Paper›PMID 28630300›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

G9a drives hypoxia-mediated gene repression for breast cancer cell survival and tumorigenesis.

Francesco Casciello, Fares Al-Ejeh, Greg Kelly, Donal J Brennan, Shin Foong Ngiow, Arabella Young, Thomas Stoll, Karolina Windloch, Michelle M Hill, Mark J Smyth and 2 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

86 citing papers in PubMed, 128 citations in OpenAlex.

  1. Article
  2. Alterations to the yeast chromatin landscape during hypoxia.bioRxiv : the preprint server for biology · 2026
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26 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 5 institutions in 2 countries.

Francesco CascielloQIMR Berghofer Medical Research Institute, Herston, QLD 4006, Australia.
Fares Al-EjehQIMR Berghofer Medical Research Institute, Herston, QLD 4006, Australia.
Greg KellyQIMR Berghofer Medical Research Institute, Herston, QLD 4006, Australia.
Donal J BrennanUniversity College Dublin School of Medicine, Catherine McCauley Research Centre, Mater Misericoridiae University Hospital, Dublin 7, Ireland.
Shin Foong NgiowQIMR Berghofer Medical Research Institute, Herston, QLD 4006, Australia.
Arabella YoungQIMR Berghofer Medical Research Institute, Herston, QLD 4006, Australia.
Thomas StollThe University of Queensland Diamantina Institute, The University of Queensland, Translational Research Institute, Woolloongabba QLD 4102, Australia.
Karolina WindlochQIMR Berghofer Medical Research Institute, Herston, QLD 4006, Australia.
Michelle M HillThe University of Queensland Diamantina Institute, The University of Queensland, Translational Research Institute, Woolloongabba QLD 4102, Australia.
Mark J SmythQIMR Berghofer Medical Research Institute, Herston, QLD 4006, Australia.
Frank GannonQIMR Berghofer Medical Research Institute, Herston, QLD 4006, Australia.
Jason S LeeQIMR Berghofer Medical Research Institute, Herston, QLD 4006, Australia; jason.lee@qimrberghofer.edu.au.ORCID 0000-0003-0879-934X
QIMR Berghofer Medical Research Institute · AUQueensland University of Technology · AUThe University of Queensland · AUTranslational Research Institute · AUUniversity College Dublin · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G9a is an epigenetic regulator that methylates H3K9, generally causing repression of gene expression, and participates in diverse cellular functions. G9a is genetically deregulated in a variety of tumor types and can silence tumor suppressor genes and, therefore, is important for carcinogenesis. Although hypoxia is recognized to be an adverse factor in tumor growth and metastasis, the role of G9a in regulating gene expression in hypoxia has not been described extensively. Here, we show that G9a protein stability is increased in hypoxia via reduced proline hydroxylation and, hence, inefficient degradation by the proteasome. This inefficiency leads to an increase in H3K9me2 at its target promoters. Blocking the methyltransferase activity of G9a inhibited cellular proliferation and migration in vitro and tumor growth in vivo. Furthermore, an increased level of G9a is a crucial factor in mediating the hypoxic response by down-regulating the expression of specific genes, including

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAntineoplastic AgentsBreast NeoplasmsCell Line, TumorCell ProliferationDisease-Free SurvivalEpigenesis, GeneticFemaleGene Expression ProfilingHistocompatibility AntigensHistone-Lysine N-MethyltransferaseHumansHypoxiaMammary Neoplasms, ExperimentalMCF-7 CellsAntineoplastic AgentsEHMT2 protein, humanHistocompatibility AntigensHistone-Lysine N-MethyltransferaseProlineRNA, Small Interferingbreast cancerepigeneticsG9ahistone methylationhypoxia

Identifiers

PMID28630300
PMCPMC5502591
OpenAlexW2677492896

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.