Evidence map›Paper›PMID 35302840›Full record

ArticleScience advances2022

H3K9 dimethylation safeguards cancer cells against activation of the interferon pathway.

Anne Meldgaard Hansen, Ying Ge, Mikkel Bruhn Schuster, Sachin Pundhir, Janus Schou Jakobsen, Adrija Kalvisa, Marta Cecylia Tapia, Sandra Gordon, Francesca Ambri, Frederik Otzen Bagger and 3 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.8field-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

28 citing papers in PubMed, 40 citations in OpenAlex.

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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

13 authors at 1 institution in 4 countries.

Anne Meldgaard HansenThe Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.ORCID 0000-0002-2215-1155
Ying GeThe Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.ORCID 0000-0003-1114-0204
Mikkel Bruhn SchusterThe Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.ORCID 0000-0003-1742-5550
Sachin PundhirThe Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.ORCID 0000-0001-9047-7280
Janus Schou JakobsenThe Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.ORCID 0000-0001-6135-5815
Adrija KalvisaThe Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.
Marta Cecylia TapiaThe Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.ORCID 0000-0001-8529-2740
Sandra GordonBiotech Research and Innovation Center (BRIC), University of Copenhagen, 2200 Copenhagen, Denmark.ORCID 0000-0003-0270-8291
Francesca AmbriBiotech Research and Innovation Center (BRIC), University of Copenhagen, 2200 Copenhagen, Denmark.ORCID 0000-0002-1999-9294
Frederik Otzen BaggerThe Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.ORCID 0000-0003-0636-8845
Deo PandeyBiotech Research and Innovation Center (BRIC), University of Copenhagen, 2200 Copenhagen, Denmark.ORCID 0000-0001-5493-3197
Kristian HelinBiotech Research and Innovation Center (BRIC), University of Copenhagen, 2200 Copenhagen, Denmark.
Bo Torben PorseThe Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.ORCID 0000-0001-6043-0844
University of Copenhagen · DK

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

Activation of interferon genes constitutes an important anticancer pathway able to restrict proliferation of cancer cells. Here, we demonstrate that the H3K9me3 histone methyltransferase (HMT) suppressor of variegation 3-9 homolog 1 (SUV39H1) is required for the proliferation of acute myeloid leukemia (AML) and find that its loss leads to activation of the interferon pathway. Mechanistically, we show that this occurs via destabilization of a complex composed of SUV39H1 and the two H3K9me2 HMTs, G9A and GLP. Indeed, loss of H3K9me2 correlated with the activation of key interferon pathway genes, and interference with the activities of G9A/GLP largely phenocopied loss of SUV39H1. Last, we demonstrate that inhibition of G9A/GLP synergized with DNA demethylating agents and that SUV39H1 constitutes a potential biomarker for the response to hypomethylation treatment. Collectively, we uncovered a clinically relevant role for H3K9me2 in safeguarding cancer cells against activation of the interferon pathway.

Identifiers

PMID35302840
PMCPMC8932663
OpenAlexW4220949003

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.