Evidence map›Paper›PMID 36073514›Full record

ArticleHaematologica2023

Activation of long non-coding RNA NEAT1 leads to survival advantage of multiple myeloma cells by supporting a positive regulatory loop with DNA repair proteins.

Elisa Taiana, Cecilia Bandini, Vanessa Katia Favasuli, Domenica Ronchetti, Ilaria Silvestris, Noemi Puccio, Katia Todoerti, Silvia Erratico, Domenica Giannandrea, Niccolò Bolli and 6 more

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 19 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

16 authors at 6 institutions in 2 countries.

Elisa TaianaHematology, Fondazione Cà Granda IRCCS Policlinico, 20122 Milan, Italy; Department of Oncology and Hemato-oncology, University of Milan, Italy 20122 Milan. elisa.taiana@unimi.it.
Cecilia BandiniDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy; Città Della Salute e della Scienza Hospital, 10126 Turin.
Vanessa Katia FavasuliHematology, Fondazione Cà Granda IRCCS Policlinico, 20122 Milan, Italy; Department of Oncology and Hemato-oncology, University of Milan, Italy 20122 Milan.
Domenica RonchettiHematology, Fondazione Cà Granda IRCCS Policlinico, 20122 Milan, Italy; Department of Oncology and Hemato-oncology, University of Milan, Italy 20122 Milan.
Ilaria SilvestrisHematology, Fondazione Cà Granda IRCCS Policlinico, 20122 Milan, Italy; Department of Oncology and Hemato-oncology, University of Milan, Italy 20122 Milan.
Noemi PuccioHematology, Fondazione Cà Granda IRCCS Policlinico, 20122 Milan, Italy; Department of Oncology and Hemato-oncology, University of Milan, Italy 20122 Milan.
Katia TodoertiHematology, Fondazione Cà Granda IRCCS Policlinico, 20122 Milan.
Silvia ErraticoNovystem Spa, Milan, Italy; Stem Cell Laboratory, Department of Pathophysiology and Transplantation, University of Milan, Centro Dino Ferrari, Unit of Neurology, Fondazione Cà Granda IRCCS Policlinico, 20122 Milan.
Domenica GiannandreaDepartment of Health Sciences, University of Milan, 20142 Milan.
Niccolò BolliHematology, Fondazione Cà Granda IRCCS Policlinico, 20122 Milan, Italy; Department of Oncology and Hemato-oncology, University of Milan, Italy 20122 Milan.
Nicola AmodioDepartment of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, 88100 Catanzaro.
Alessia CiarrocchiLaboratory of Translational Research, Azienda Unità Sanitaria Locale-IRCCS Reggio Emilia, 42123 Reggio Emilia.
Raffaella ChiaramonteDepartment of Health Sciences, University of Milan, 20142 Milan.
Yvan TorrenteStem Cell Laboratory, Department of Pathophysiology and Transplantation, University of Milan, Centro Dino Ferrari, Unit of Neurology, Fondazione Cà Granda IRCCS Policlinico, 20122 Milan.
Roberto PivaDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy; Città Della Salute e della Scienza Hospital, 10126 Turin.
Antonino NeriHematology, Fondazione Cà Granda IRCCS Policlinico, 20122 Milan, Italy; Department of Oncology and Hemato-oncology, University of Milan, Italy 20122 Milan. antonino.neri@unimi.it.
University of Milan · ITFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITAzienda Ospedaliera Citta' della Salute e della Scienza di Torino · ITAzienda Sanitaria Unità Locale di Reggio Emilia · ITDepartment of Medical Sciences · RUMagna Graecia University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNA NEAT1 is the core structural component of the nuclear paraspeckle (PS) organelles and it has been found to be deregulated in multiple myeloma (MM) patients. Experimental evidence indicated that NEAT1 silencing negatively impacts proliferation and viability of MM cells, both in vitro and in vivo, suggesting a role in DNA damage repair (DDR). In order to elucidate the biological and molecular relevance of NEAT1 upregulation in MM disease we exploited the CRISPR/Cas9 synergistic activation mediator genome editing system to engineer the AMO-1 MM cell line and generate two clones that para-physiologically transactivate NEAT1 at different levels. NEAT1 overexpression is associated with oncogenic and prosurvival advantages in MM cells exposed to nutrient starvation or a hypoxic microenvironment, which are stressful conditions often associated with more aggressive disease phases. Furthermore, we highlighted the NEAT1 involvement in virtually all DDR processes through, at least, two different mechanisms. On one side NEAT1 positively regulates the posttranslational stabilization of essential PS proteins, which are involved in almost all DDR systems, thus increasing their availability within cells. On the other hand, NEAT1 plays a crucial role as a major regulator of a molecular axis that includes ATM and the catalytic subunit of DNA-PK kinase proteins, and their direct targets pRPA32 and pCHK2. Overall, we provided novel important insightsthe role of NEAT1 in supporting MM cells adaptation to stressful conditions by improving the maintenance of DNA integrity. Taken together, our results suggest that NEAT1, and probably PS organelles, could represent a potential therapeutic target for MM treatment.

Indexed as

MicroRNAsMultiple MyelomaRNA, Long NoncodingCell Line, TumorDNA RepairHumansTranscriptional ActivationTumor MicroenvironmentUp-RegulationMicroRNAsNEAT1 long non-coding RNA, humanRNA, Long Noncoding

Identifiers

PMID36073514
PMCPMC9827177
OpenAlexW4294991559

What OpenQuestion holds

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Registered trials

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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.