Evidence map›Paper›PMID 29487387›Full record

ArticleLeukemia2018

Drugging the lncRNA MALAT1 via LNA gapmeR ASO inhibits gene expression of proteasome subunits and triggers anti-multiple myeloma activity.

Nicola Amodio, Maria Angelica Stamato, Giada Juli, Eugenio Morelli, Mariateresa Fulciniti, Martina Manzoni, Elisa Taiana, Luca Agnelli, Maria Eugenia Gallo Cantafio, Enrica Romeo and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 175 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
175citing papers in PubMed, 1 pooled it
9.8field-weighted citation impact, top 1% 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

175 citing papers in PubMed, 1 synthesis or guideline pooled it, 244 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. RNA therapeutics: current status and future directions.Signal transduction and targeted therapy · 2026
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  7. Article
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  10. Advances in antisense oligonucleotide treatment for cancer.Japanese journal of clinical oncology · 2026
    Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Knocking Down Long Noncoding RNAs Using Antisense Oligonucleotide Gapmers.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  16. Review
  17. Review
  18. Review
  19. Gapmers: Invention and Early History.Methods in molecular biology (Clifton, N.J.) · 2026
    Review
  20. Article

115 more citing papers are in PubMed but not listed here.

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

18 authors at 6 institutions in 2 countries.

Nicola AmodioDepartment of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, Catanzaro, Italy.
Maria Angelica StamatoDepartment of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, Catanzaro, Italy.
Giada JuliDepartment of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, Catanzaro, Italy.
Eugenio MorelliDepartment of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, Catanzaro, Italy.
Mariateresa FulcinitiJerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Martina ManzoniDepartment of Oncology and Hemato-oncology, University of Milan, Milan, Italy.
Elisa TaianaDepartment of Oncology and Hemato-oncology, University of Milan, Milan, Italy.
Luca AgnelliDepartment of Oncology and Hemato-oncology, University of Milan, Milan, Italy.
Maria Eugenia Gallo CantafioDepartment of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, Catanzaro, Italy.
Enrica RomeoDepartment of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, Catanzaro, Italy.
Lavinia RaimondiLaboratory of Tissue Engineering, Rizzoli Orthopedic Institute, Palermo, Italy.
Daniele CaraccioloDepartment of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, Catanzaro, Italy.
Valeria ZuccalàPathology Unit, Pugliese-Ciaccio Hospital, Catanzaro, Italy.
Marco RossiDepartment of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, Catanzaro, Italy.
Antonino NeriDepartment of Oncology and Hemato-oncology, University of Milan, Milan, Italy.
Nikhil C MunshiJerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Pierosandro TagliaferriDepartment of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, Catanzaro, Italy.
Pierfrancesco TassoneDepartment of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, Catanzaro, Italy. tassone@unicz.it.
Magna Graecia University · ITFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITUniversity of Milan · ITAzienda Ospedaliera Pugliese Ciaccio · ITDana-Farber Cancer Institute · USVA Boston Healthcare System · US

Funding

MOLECULAR MANIPULATION TO ENHANCE ANTI-MYELOMA RESPONSEI01BX001584 · VA · VA BOSTON HEALTH CARE SYSTEM · PI MUNSHI, NIKHIL C. · 2013 to 2025
–
BLRD VA I01 BX001584
6 · The paper itself

Abstract

The biological role and therapeutic potential of long non-coding RNAs (lncRNAs) in multiple myeloma (MM) are still to be investigated. Here, we studied the functional significance and the druggability of the oncogenic lncRNA MALAT1 in MM. Targeting MALAT1 by novel LNA-gapmeR antisense oligonucleotide antagonized MM cell proliferation and triggered apoptosis both in vitro and in vivo in a murine xenograft model of human MM. Of note, antagonism of MALAT1 downmodulated the two major transcriptional activators of proteasome subunit genes, namely NRF1 and NRF2, and resulted in reduced trypsin, chymotrypsin and caspase-like proteasome activities and in accumulation of polyubiquitinated proteins. NRF1 and NRF2 decrease upon MALAT1 targeting was due to transcriptional activation of their negative regulator KEAP1, and resulted in reduced expression of anti-oxidant genes and increased ROS levels. In turn, NRF1 promoted MALAT1 expression thus establishing a positive feedback loop. Our findings demonstrate a crucial role of MALAT1 in the regulation of the proteasome machinery, and provide proof-of-concept that its targeting is a novel powerful option for the treatment of MM.

Indexed as

Gene Expression Regulation, NeoplasticRNA InterferenceApoptosisCaspasesCell ProliferationEpigenesis, GeneticHumansModels, BiologicalMultiple MyelomaNF-E2-Related Factor 2Nuclear Respiratory Factor 1Oligonucleotides, AntisenseProteasome Endopeptidase ComplexProtein SubunitsReactive Oxygen SpeciesRNA, Long NoncodingCaspasesMALAT1 long non-coding RNA, humanNFE2L2 protein, humanNF-E2-Related Factor 2NRF1 protein, humanNuclear Respiratory Factor 1Oligonucleotides, AntisenseProteasome Endopeptidase ComplexProtein SubunitsReactive Oxygen SpeciesRNA, Long Noncoding

Identifiers

PMID29487387
PMCPMC6127082
OpenAlexW2794096909

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.