Evidence map›Paper›PMID 25492890›Full record

ArticleNucleic acids research2015

The high mobility group A2 protein epigenetically silences the Cdh1 gene during epithelial-to-mesenchymal transition.

E-Jean Tan, Kaoru Kahata, Oskar Idås, Sylvie Thuault, Carl-Henrik Heldin, Aristidis Moustakas

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

41 citing papers in PubMed, 65 citations in OpenAlex.

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  7. Landscape of NcRNAs involved in drug resistance of breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
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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

6 authors at 3 institutions in 1 country.

E-Jean TanLudwig Institute for Cancer Research, Science for Life Laboratory, Uppsala University, Uppsala SE-75124, Sweden.
Kaoru KahataLudwig Institute for Cancer Research, Science for Life Laboratory, Uppsala University, Uppsala SE-75124, Sweden.
Oskar IdåsLudwig Institute for Cancer Research, Science for Life Laboratory, Uppsala University, Uppsala SE-75124, Sweden.
Sylvie ThuaultLudwig Institute for Cancer Research, Science for Life Laboratory, Uppsala University, Uppsala SE-75124, Sweden.
Carl-Henrik HeldinLudwig Institute for Cancer Research, Science for Life Laboratory, Uppsala University, Uppsala SE-75124, Sweden.
Aristidis MoustakasLudwig Institute for Cancer Research, Science for Life Laboratory, Uppsala University, Uppsala SE-75124, Sweden Department of Medical Biochemistry and Microbiology, Science for Life Laboratory, Uppsala University, Uppsala SE-75123, Sweden aris.moustakas@imbim.uu.se.
Uppsala University · SELudwig Cancer Research · SEScience for Life Laboratory · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The loss of the tumour suppressor E-cadherin (Cdh1) is a key event during tumourigenesis and epithelial-mesenchymal transition (EMT). Transforming growth factor-β (TGFβ) triggers EMT by inducing the expression of non-histone chromatin protein High Mobility Group A2 (HMGA2). We have previously shown that HMGA2, together with Smads, regulate a network of EMT-transcription factors (EMT-TFs) like Snail1, Snail2, ZEB1, ZEB2 and Twist1, most of which are well-known repressors of the Cdh1 gene. In this study, we show that the Cdh1 promoter is hypermethylated and epigenetically silenced in our constitutive EMT cell model, whereby HMGA2 is ectopically expressed in mammary epithelial NMuMG cells and these cells are highly motile and invasive. Furthermore, HMGA2 remodels the chromatin to favour binding of de novo DNA methyltransferase 3A (DNMT3A) to the Cdh1 promoter. E-cadherin expression could be restored after treatment with the DNA de-methylating agent 5-aza-2'-deoxycytidine. Here, we describe a new epigenetic role for HMGA2, which follows the actions that HMGA2 initiates via the EMT-TFs, thus achieving sustained silencing of E-cadherin expression and promoting tumour cell invasion.

Indexed as

Gene SilencingAntigens, CDAzacitidineBreast NeoplasmsCadherinsCCCTC-Binding FactorCell Line, TumorCell MovementCells, CulturedCpG IslandsDecitabineDNA (Cytosine-5-)-MethyltransferasesDNA MethylationDNA Methyltransferase 3AEpithelial-Mesenchymal TransitionFemaleAntigens, CDAzacitidineCadherinsCCCTC-Binding FactorCDH1 protein, humanCTCF protein, humanDecitabineDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNMT3A protein, humanHMGA2 ProteinRepressor ProteinsTransforming Growth Factor beta

Identifiers

PMID25492890
PMCPMC4288184
OpenAlexW2150585673

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.