Evidence map›Paper›PMID 35016717›Full record

ArticleJournal of experimental & clinical cancer research : CR2022

MiR-423-5p prevents MALAT1-mediated proliferation and metastasis in prostate cancer.

Carmela Ferri, Anna Di Biase, Marco Bocchetti, Silvia Zappavigna, Sarah Wagner, Pauline Le Vu, Amalia Luce, Alessia Maria Cossu, Jayakumar Vadakekolathu, Amanda Miles and 8 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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  10. Fluorescence imaging of MALAT1 expression using a Cy5.5-labeled antisense oligonucleotide in lung cancer and epidermal carcinoma cells.Cancer imaging : the official publication of the International Cancer Imaging Society · 2025
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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

18 authors at 6 institutions in 2 countries.

Carmela Ferri *Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Via L. De Crecchio, 7, 80138, Naples, Italy.
Anna Di Biase *The John van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Lane, Nottingham, NG11 8NS, UK.
Marco BocchettiDepartment of Precision Medicine, University of Campania "Luigi Vanvitelli", Via L. De Crecchio, 7, 80138, Naples, Italy.
Silvia ZappavignaDepartment of Precision Medicine, University of Campania "Luigi Vanvitelli", Via L. De Crecchio, 7, 80138, Naples, Italy.
Sarah WagnerThe John van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Lane, Nottingham, NG11 8NS, UK.
Pauline Le VuClinical and Experimental Sciences, Faculty of Medicine, Southampton General Hospital, University of Southampton, Coxford Rd, Southampton, SO16 5YA, UK.
Amalia LuceDepartment of Precision Medicine, University of Campania "Luigi Vanvitelli", Via L. De Crecchio, 7, 80138, Naples, Italy.
Alessia Maria CossuLaboratory of Precision and Molecular Oncology, Biogem Scarl, Institute of Genetic Research, Contrada Camporeale, 83031, Ariano Irpino, Italy.
Jayakumar VadakekolathuThe John van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Lane, Nottingham, NG11 8NS, UK.
Amanda MilesThe John van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Lane, Nottingham, NG11 8NS, UK.
David J BoocockThe John van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Lane, Nottingham, NG11 8NS, UK.
Alex RobinsonDepartment of Life Sciences, Faculty of Health, Education and Life Sciences, Birmingham City University, Birmingham, B15 3TN, UK.
Melanie SchwerdtfegerDepartment of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138, Naples, Italy.
Virginia TirinoDepartment of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138, Naples, Italy.
Federica PapaccioDepartment of Medicine, Surgery and Dentistry "Scuola Medica Salernitana", University of Salerno, Via S. Allende, 84081, Baronissi, Italy.
Michele Caraglia *Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Via L. De Crecchio, 7, 80138, Naples, Italy. michele.caraglia@unicampania.it.ORCID http://orcid.org/0000-0003-2408-6091
Tarik Regad *Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Via L. De Crecchio, 7, 80138, Naples, Italy.
Vincenzo Desiderio *Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138, Naples, Italy. vincenzo.desiderio@unicampania.it.
University of Campania "Luigi Vanvitelli" · ITNottingham Trent University · GBBiogem · ITBirmingham City University · GBSouthampton General Hospital · GBUniversity of Salerno · IT

Funding

associazione italiana per la ricerca sul cancro IG 20711
6 · The paper itself

Abstract

backgroundThe long non-coding RNA (lncRNA), MALAT1, plays a key role in the development of different cancers, and its expression is associated with worse prognosis in patients. However, its mechanism of action and its regulation are not well known in prostate cancer (PCa). A general mechanism of action of lncRNAs is their interaction with other epigenetic regulators including microRNAs (miRNAs).

methodsUsing lentiviral stable miRNA transfection together with cell biology functional assays and gene expression/target analysis, we investigated the interaction between MALAT1 and miR-423-5p, defined as a target with in silico prediction analysis, in PCa.

resultsThrough bioinformatic analysis of data available from TCGA, we have found that MALAT1 expression correlates with high Gleason grade, metastasis occurrence, and reduced survival in PCa patients. These findings were validated on a TMA of PCa showing a significant correlation between MALAT1 expression with both stage and grading. We report that, in PCa cells, MALAT1 expression and activity is regulated by miR-423-5p that binds MALAT1, downregulates its expression and inhibits its activity in promoting proliferation, migration, and invasion. Using NanoString analysis, we unraveled downstream cell pathways that were affected by miR-423-5p expression and MALAT1 downregulation and identified several alterations in genes that are involved in metastatic response and angiogenic pathways. In addition, we showed that the overexpression of miR-423-5p increases survival and decreases metastases formation in a xenograft mouse model.

conclusionsWe provide evidence on the role of MALAT1 in PCa tumorigenesis and progression. Also, we identify a direct interaction between miR-423-5p and MALAT1, which results in the suppression of MALAT1 action in PCa.

Indexed as

AnimalsCell ProliferationHumansMaleMiceMice, NudeMicroRNAsNeoplasm MetastasisProstatic NeoplasmsTransfectionMicroRNAsMirn423 microRNA, mouseCancerCellular biologyGene expressionlncRNAsMalat-1miR-423-5pmiRNAsMolecular biologyProstate

Identifiers

PMID35016717
PMCPMC8751098
OpenAlexW4205413657

What OpenQuestion holds

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LicenceCC BY
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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.