Evidence map›Paper›PMID 33960111›Full record

ArticleEMBO reports2021

HOTAIR lncRNA promotes epithelial-mesenchymal transition by redistributing LSD1 at regulatory chromatin regions.

Julien Jarroux, Dominika Foretek, Claire Bertrand, Marc Gabriel, Ugo Szachnowski, Zohra Saci, Shuling Guo, Arturo Londoño-Vallejo, Marina Pinskaya, Antonin Morillon

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 49 citations in OpenAlex.

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  20. LncRNAs in oncogenic microenvironment: from threat to therapy.Frontiers in cell and developmental biology · 2024
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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

10 authors at 2 institutions in 2 countries.

Julien JarrouxncRNA, Epigenetic and Genome Fluidity, CNRS UMR3244, Sorbonne Université, PSL University, Institut Curie, Centre de Recherche, Paris, France.
Dominika ForetekncRNA, Epigenetic and Genome Fluidity, CNRS UMR3244, Sorbonne Université, PSL University, Institut Curie, Centre de Recherche, Paris, France.ORCID 0000-0002-2231-1710
Claire BertrandncRNA, Epigenetic and Genome Fluidity, CNRS UMR3244, Sorbonne Université, PSL University, Institut Curie, Centre de Recherche, Paris, France.
Marc GabrielncRNA, Epigenetic and Genome Fluidity, CNRS UMR3244, Sorbonne Université, PSL University, Institut Curie, Centre de Recherche, Paris, France.
Ugo SzachnowskincRNA, Epigenetic and Genome Fluidity, CNRS UMR3244, Sorbonne Université, PSL University, Institut Curie, Centre de Recherche, Paris, France.
Zohra SacincRNA, Epigenetic and Genome Fluidity, CNRS UMR3244, Sorbonne Université, PSL University, Institut Curie, Centre de Recherche, Paris, France.
Shuling GuoIonis Pharmaceuticals, Inc, Carlsbad, CA, USA.
Arturo Londoño-VallejoTelomeres and Cancer, CNRS UMR3244, Sorbonne Université, PSL Université, Institut Curie, Centre de Recherche, Paris, France.ORCID 0000-0003-3535-7563
Marina PinskayancRNA, Epigenetic and Genome Fluidity, CNRS UMR3244, Sorbonne Université, PSL University, Institut Curie, Centre de Recherche, Paris, France.ORCID 0000-0003-1992-0264
Antonin MorillonncRNA, Epigenetic and Genome Fluidity, CNRS UMR3244, Sorbonne Université, PSL University, Institut Curie, Centre de Recherche, Paris, France.ORCID 0000-0002-0575-5264
Centre National de la Recherche Scientifique · FRIonis Pharmaceuticals (United States) · US

Funding

European Research Council DARK-616180-ERC-2014
6 · The paper itself

Abstract

Epithelial-to-mesenchymal transition (EMT) describes the loss of epithelial traits and gain of mesenchymal traits by normal cells during development and by neoplastic cells during cancer metastasis. The long noncoding RNA HOTAIR triggers EMT, in part by serving as a scaffold for PRC2 and thus promoting repressive histone H3K27 methylation. In addition to PRC2, HOTAIR interacts with the LSD1 lysine demethylase, an epigenetic regulator of cell fate during development and differentiation, but little is known about the role of LSD1 in HOTAIR function during EMT. Here, we show that HOTAIR requires its LSD1-interacting domain, but not its PRC2-interacting domain, to promote the migration of epithelial cells. This activity is suppressed by LSD1 overexpression. LSD1-HOTAIR interactions induce partial reprogramming of the epithelial transcriptome altering LSD1 distribution at promoter and enhancer regions. Thus, we uncover an unexpected role of HOTAIR in EMT as an LSD1 decommissioning factor, counteracting its activity in the control of epithelial identity.

Indexed as

RNA, Long NoncodingCell Line, TumorChromatinEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHistone DemethylasesHistonesHumansChromatinHistone DemethylasesHistonesHOTAIR long untranslated RNA, humanKDM1A protein, humanRNA, Long NoncodingEMTenhancerHOTAIRLSD1promoter

Identifiers

PMID33960111
PMCPMC8366456
OpenAlexW3157928350

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.