Evidence map›Paper›PMID 31101765›Full record

ArticleCancer research2019

miR-450a Acts as a Tumor Suppressor in Ovarian Cancer by Regulating Energy Metabolism.

Bruna Rodrigues Muys, Josane F Sousa, Jessica Rodrigues Plaça, Luíza Ferreira de Araújo, Aishe A Sarshad, Dimitrios G Anastasakis, Xiantao Wang, Xiao Ling Li, Greice Andreotti de Molfetta, Anelisa Ramão and 4 more

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 68 citations in OpenAlex.

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  16. Circular RNAs in organ injury: recent development.Journal of translational medicine · 2022
    Review
  17. MicroRNAs as Regulators of Cancer Cell Energy Metabolism.Journal of personalized medicine · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 3 countries.

Bruna Rodrigues MuysDepartment of Genetics, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.ORCID 0000-0002-3963-0865
Josane F SousaDepartment of Genetics, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Jessica Rodrigues PlaçaDepartment of Genetics, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Luíza Ferreira de AraújoDepartment of Genetics, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Aishe A SarshadLaboratory of Muscle Stem Cells and Gene Regulation, National Institute for Arthritis and Musculoskeletal and Skin Disease, Bethesda, Maryland.
Dimitrios G AnastasakisLaboratory of Muscle Stem Cells and Gene Regulation, National Institute for Arthritis and Musculoskeletal and Skin Disease, Bethesda, Maryland.
Xiantao WangLaboratory of Muscle Stem Cells and Gene Regulation, National Institute for Arthritis and Musculoskeletal and Skin Disease, Bethesda, Maryland.
Xiao Ling LiRegulatory RNAs and Cancer Section, Genetics Branch, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
Greice Andreotti de MolfettaDepartment of Genetics, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Anelisa RamãoDepartment of Genetics, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.ORCID 0000-0001-5958-3341
Ashish LalRegulatory RNAs and Cancer Section, Genetics Branch, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
Daniel Onofre VidalMolecular Oncology Research Center, Barretos Cancer Hospital, Barretos, Brazil.
Markus HafnerLaboratory of Muscle Stem Cells and Gene Regulation, National Institute for Arthritis and Musculoskeletal and Skin Disease, Bethesda, Maryland. markus.hafner@nih.gov wilsonjr@usp.br.ORCID 0000-0002-4336-6518
Wilson A SilvaDepartment of Genetics, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil. markus.hafner@nih.gov wilsonjr@usp.br.ORCID 0000-0001-9364-2886
Universidade de Ribeirão Preto · BRNational Institute of Arthritis and Musculoskeletal and Skin Diseases · USCenter for Cancer Research · USHospital de Câncer de Barretos · BR

Funding

Role of long non-coding RNAs in p53 signalingZIABC011646 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LAL, ASHISH · 2015 to 2025
$15.0M
Integration of the results from systems-level determination of cis-acting elements into high-resolution maps of posttranscriptional regulatory events.ZIAAR041205 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI HAFNER, MARKUS · 2016 to 2025
$5.5M
The role of AU-rich element binding proteins in shaping target mRNA expressionZIAAR041200 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI HAFNER, MARKUS · 2014 to 2023
$5.1M
Intramural NIH HHS Z99 AR999999
6 · The paper itself

Abstract

Dysregulation of miRNA expression is associated with multiple diseases, including cancers, in which small RNAs can have either oncogenic or tumor suppressive functions. Here we investigated the potential tumor suppressive function of miR-450a, one of the most significantly downregulated miRNAs in ovarian cancer. RNA-seq analysis of the ovarian cancer cell line A2780 revealed that overexpression of miR-450a suppressed multiple genes involved in the epithelial-to-mesenchymal transition (EMT). Overexpression of miR-450a reduced tumor migration and invasion and increased anoikis in A2780 and SKOV-3 cell lines and reduced tumor growth in an ovarian tumor xenographic model. Combined AGO-PAR-CLIP and RNA-seq analysis identified a panel of potential miR-450a targets, of which many, including TIMMDC1, MT-ND2, ACO2, and ATP5B, regulate energetic metabolism. Following glutamine withdrawal, miR-450a overexpression decreased mitochondrial membrane potential but increased glucose uptake and viability, characteristics of less invasive ovarian cancer cell lines. In summary, we propose that miR-450a acts as a tumor suppressor in ovarian cancer cells by modulating targets associated with glutaminolysis, which leads to decreased production of lipids, amino acids, and nucleic acids, as well as inhibition of signaling pathways associated with EMT. SIGNIFICANCE: miR-450a limits the metastatic potential of ovarian cancer cells by targeting a set of mitochondrial mRNAs to reduce glycolysis and glutaminolysis.

Indexed as

Energy MetabolismEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticAconitate HydrataseAnimalsApoptosisBiomarkers, TumorCell CycleCell MovementCell ProliferationFemaleHumansMembrane Potential, MitochondrialMiceMice, Inbred NODMice, SCIDACO2 protein, humanAconitate HydrataseATP5F1B protein, humanBiomarkers, TumorMicroRNAsMIRN450 microRNA, humanMitochondrial Membrane Transport ProteinsMitochondrial Precursor Protein Import Complex ProteinsMitochondrial Proton-Translocating ATPasesNADH DehydrogenaseNADH dehydrogenase subunit 2, humanTIMMDC1 protein, human

Identifiers

PMID31101765
PMCPMC6606360
OpenAlexW2946599769

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.