Evidence map›Paper›PMID 35776213›Full record

ArticleCellular and molecular life sciences : CMLS2022

ALYREF, a novel factor involved in breast carcinogenesis, acts through transcriptional and post-transcriptional mechanisms selectively regulating the short NEAT1 isoform.

Christiane Klec, Erik Knutsen, Daniela Schwarzenbacher, Katharina Jonas, Barbara Pasculli, Ellen Heitzer, Beate Rinner, Katarina Krajina, Felix Prinz, Benjamin Gottschalk and 11 more

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.1field-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

33 citing papers in PubMed, 44 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

21 authors at 4 institutions in 4 countries.

Christiane KlecDivision of Oncology, Department of Internal Medicine, Medical University of Graz, Augenbruggerplatz 15, 8010, Graz, Austria.
Erik KnutsenDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
Daniela SchwarzenbacherDivision of Oncology, Department of Internal Medicine, Medical University of Graz, Augenbruggerplatz 15, 8010, Graz, Austria.
Katharina JonasDivision of Oncology, Department of Internal Medicine, Medical University of Graz, Augenbruggerplatz 15, 8010, Graz, Austria.
Barbara PasculliFondazione IRCCS Casa Sollievo della Sofferenza Laboratorio di Oncologia, San Giovanni Rotondo, FG, Italy.
Ellen HeitzerInstitute of Human Genetics, Medical University of Graz (MUG), Graz, Austria.
Beate RinnerBiomedical Research, Medical University of Graz (MUG), Graz, Austria.
Katarina KrajinaDivision of Oncology, Department of Internal Medicine, Medical University of Graz, Augenbruggerplatz 15, 8010, Graz, Austria.
Felix PrinzDivision of Oncology, Department of Internal Medicine, Medical University of Graz, Augenbruggerplatz 15, 8010, Graz, Austria.
Benjamin GottschalkMolecular Biology and Biochemistry, Gottfried Schatz Research Center for Cellular Signaling, Metabolism and Aging, Medical University of Graz (MUG), Graz, Austria.
Peter UlzInstitute of Human Genetics, Medical University of Graz (MUG), Graz, Austria.
Alexander DeutschDivision of Hematology, Department of Internal Medicine, Medical University of Graz (MUG), Graz, Austria.
Andreas ProkeschDivision of Cell Biology, Histology and Embryology, Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Medical University of Graz, Graz, Austria.
Stephan W JahnInstitute of Pathology, Diagnostic and Research Center for Molecular BioMedicine, Medical University of Graz, Graz, Austria.
S Mohammad LellahiDepartment of Medical Biology, Faculty of Health Sciences, UiT-the Arctic University of Norway, Tromsö, Norway.
Maria PeranderDepartment of Medical Biology, Faculty of Health Sciences, UiT-the Arctic University of Norway, Tromsö, Norway.
Raffaela BarbanoFondazione IRCCS Casa Sollievo della Sofferenza Laboratorio di Oncologia, San Giovanni Rotondo, FG, Italy.
Wolfgang F GraierMolecular Biology and Biochemistry, Gottfried Schatz Research Center for Cellular Signaling, Metabolism and Aging, Medical University of Graz (MUG), Graz, Austria.
Paola ParrellaFondazione IRCCS Casa Sollievo della Sofferenza Laboratorio di Oncologia, San Giovanni Rotondo, FG, Italy.
George Adrian CalinDepartment of Translational Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Martin PichlerDivision of Oncology, Department of Internal Medicine, Medical University of Graz, Augenbruggerplatz 15, 8010, Graz, Austria. martin.pichler@medunigraz.at.ORCID http://orcid.org/0000-0002-8701-9462
Medical University of Graz · ATCasa Sollievo della Sofferenza · ITThe University of Texas MD Anderson Cancer Center · USUiT The Arctic University of Norway · NO

Funding

Austrian Science Fund FWF T 1112Austrian Science Fund FWF W 1226
6 · The paper itself

Abstract

The RNA-binding protein ALYREF (THOC4) is involved in transcriptional regulation and nuclear mRNA export, though its role and molecular mode of action in breast carcinogenesis are completely unknown. Here, we identified high ALYREF expression as a factor for poor survival in breast cancer patients. ALYREF significantly influenced cellular growth, apoptosis and mitochondrial energy metabolism in breast cancer cells as well as breast tumorigenesis in orthotopic mouse models. Transcriptional profiling, phenocopy and rescue experiments identified the short isoform of the lncRNA NEAT1 as a molecular trigger for ALYREF effects in breast cancer. Mechanistically, we found that ALYREF binds to the NEAT1 promoter region to enhance the global NEAT1 transcriptional activity. Importantly, by stabilizing CPSF6, a protein that selectively activates the post-transcriptional generation of the short isoform of NEAT1, as well as by direct binding and stabilization of the short isoform of NEAT1, ALYREF selectively fine-tunes the expression of the short NEAT1 isoform. Overall, our study describes ALYREF as a novel factor contributing to breast carcinogenesis and identifies novel molecular mechanisms of regulation the two isoforms of NEAT1.

Indexed as

Breast NeoplasmsNuclear ProteinsRNA-Binding ProteinsRNA, Long NoncodingTranscription FactorsAnimalsCell Transformation, NeoplasticFemaleHumansMiceProtein IsoformsRNA TransportALYREF protein, humanNEAT1 long non-coding RNA, humanNuclear ProteinsProtein IsoformsRNA-Binding ProteinsRNA, Long NoncodingTranscription FactorsALYREFBreast cancerlncRNANEAT1Transcriptional regulation

Identifiers

PMID35776213
PMCPMC9249705
OpenAlexW4283764300

What Socratic 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 Socratic graph.