Evidence map›Paper›PMID 33375130›Full record

ArticleCancers2020

Metabolic Reprogramming by Malat1 Depletion in Prostate Cancer.

Simona Nanni, Aurora Aiello, Chiara Salis, Agnese Re, Chiara Cencioni, Lorenza Bacci, Francesco Pierconti, Francesco Pinto, Cristian Ripoli, Paola Ostano and 11 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

21 citing papers in PubMed, 25 citations in OpenAlex.

  1. Keap1-Inhibitory Peptides fromMolecules (Basel, Switzerland) · 2026
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  20. Associations between LncRNADiagnostics (Basel, Switzerland) · 2021
    Article
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 1 country.

Simona NanniFondazione Policlinico Universitario A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.
Aurora AielloNational Research Council (CNR)-IASI, Department of Engineering, ICT and Technologies for Energy and Transportation, 00185 Rome, Italy.ORCID 0000-0002-8303-1528
Chiara SalisDepartment of Translational Medicine and Surgery, Università Cattolica del Sacro Cuore Rome, 00168 Rome, Italy.
Agnese ReNational Research Council (CNR)-IASI, Department of Engineering, ICT and Technologies for Energy and Transportation, 00185 Rome, Italy.
Chiara CencioniNational Research Council (CNR)-IASI, Department of Engineering, ICT and Technologies for Energy and Transportation, 00185 Rome, Italy.
Lorenza BacciDepartment of Translational Medicine and Surgery, Università Cattolica del Sacro Cuore Rome, 00168 Rome, Italy.
Francesco PiercontiFondazione Policlinico Universitario A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.
Francesco PintoFondazione Policlinico Universitario A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.
Cristian RipoliFondazione Policlinico Universitario A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.
Paola OstanoFondazione Edo ed Elvo Tempia, 13900 Biella, Italy.ORCID 0000-0002-4000-2954
Silvia BaroniFondazione Policlinico Universitario A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.
Giacomo LazzarinoUniCamillus-Saint Camillus International University of Health Sciences (Università Cattolica del Sacro Cuore Rome), 00131 Rome, Italy.ORCID 0000-0003-1639-0966
Barbara TavazziFondazione Policlinico Universitario A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.ORCID 0000-0001-8743-0895
Dario PuglieseDepartment of Translational Medicine and Surgery, Università Cattolica del Sacro Cuore Rome, 00168 Rome, Italy.
PierFrancesco BassiFondazione Policlinico Universitario A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.
Claudio GrassiFondazione Policlinico Universitario A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.ORCID 0000-0001-7253-1685
Simona PanunziNational Research Council (CNR)-IASI, Department of Engineering, ICT and Technologies for Energy and Transportation, 00185 Rome, Italy.ORCID 0000-0003-0956-8578
Giovanna ChiorinoFondazione Edo ed Elvo Tempia, 13900 Biella, Italy.
Alfredo PontecorviFondazione Policlinico Universitario A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.
Carlo GaetanoIstituti Clinici Scientifici Maugeri, 27100 Pavia, Italy.
Antonella FarsettiNational Research Council (CNR)-IASI, Department of Engineering, ICT and Technologies for Energy and Transportation, 00185 Rome, Italy.ORCID 0000-0002-8603-7925
Università Cattolica del Sacro Cuore · ITNational Research Council · ITFondazione Edo ed Elvo Tempia · ITIstituti Clinici Scientifici Maugeri · IT

Funding

ASSOCIAZIONE ITALIANA PER LA RICERCA SUL CANCRO AIRC IG 2019- grant number ID 22858 projectEU-CardioRNA COST ACTION CA17129ITALIAN MINISTRY OF EDUCATION, UNIVERSITY AND RESEARCH PRIN2015HPMLFYITALIAN MINISTRY OF EDUCATION, UNIVERSITY AND RESEARCH PRIN2017S55RXBITALIAN MINISTRY OF HEALTH Progetto di Rete Cardiovascolare IRCCSITALIAN MINISTRY OF HEALTH RF 2010-2318330ITALIAN MINISTRY OF HEALTH RicercaCorrenteRegioneLombardia IMMUNHU
6 · The paper itself

Abstract

The lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) promotes growth and progression in prostate cancer (PCa); however, little is known about its possible impact in PCa metabolism. The aim of this work has been the assessment of the metabolic reprogramming associated with MALAT1 silencing in human PCa cells and in an ex vivo model of organotypic slice cultures (OSCs). Cultured cells and OSCs derived from primary tumors were transfected with MALAT1 specific gapmers. Cell growth and survival, gene profiling, and evaluation of targeted metabolites and metabolic enzymes were assessed. Computational analysis was made considering expression changes occurring in metabolic markers following MALAT1 targeting in cultured OSCs. MALAT1 silencing reduced expression of some metabolic enzymes, including malic enzyme 3, pyruvate dehydrogenase kinases 1 and 3, and choline kinase A. Consequently, PCa metabolism switched toward a glycolytic phenotype characterized by increased lactate production paralleled by growth arrest and cell death. Conversely, the function of mitochondrial succinate dehydrogenase and the expression of oxidative phosphorylation enzymes were markedly reduced. A similar effect was observed in OSCs. Based on this, a predictive algorithm was developed aimed to predict tumor recurrence in a subset of patients. MALAT1 targeting by gapmer delivery restored normal metabolic energy pathway in PCa cells and OSCs.

Indexed as

biomarkerslong non-coding RNAMALAT1metabolic reprogrammingmetabolismprecision medicinepredictive modelprostate cancertranscription

Identifiers

PMID33375130
PMCPMC7801945
OpenAlexW3115692566

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.