Evidence map›Paper›PMID 33610185›Full record

ArticleJournal of biomedical science2021

Glutaminase isoforms expression switches microRNA levels and oxidative status in glioblastoma cells.

Juan de Los Santos-Jiménez, José A Campos-Sandoval, Clara Márquez-Torres, Nieves Urbano-Polo, David Brøndegaard, Mercedes Martín-Rufián, Carolina Lobo, Ana Peñalver, María C Gómez-García, Janet Martín-Campos and 11 more

Open access · diamondAbstract read
In one paragraph

Article in Journal of biomedical science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

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  18. Metabolic Rewiring in Glioblastoma Cancer:Frontiers in oncology · 2022
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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

21 authors at 5 institutions in 3 countries.

Juan de Los Santos-JiménezDepartamento de Biología Molecular y Bioquímica and Instituto de Investigación de Biomedicina de Málaga (IBIMA), Universidad de Málaga, Málaga, Spain.
José A Campos-SandovalDepartamento de Biología Molecular y Bioquímica and Instituto de Investigación de Biomedicina de Málaga (IBIMA), Universidad de Málaga, Málaga, Spain.
Clara Márquez-TorresDepartamento de Biología Molecular y Bioquímica and Instituto de Investigación de Biomedicina de Málaga (IBIMA), Universidad de Málaga, Málaga, Spain.
Nieves Urbano-PoloDepartamento de Biología Molecular y Bioquímica and Instituto de Investigación de Biomedicina de Málaga (IBIMA), Universidad de Málaga, Málaga, Spain.
David BrøndegaardDepartamento de Biología Molecular y Bioquímica and Instituto de Investigación de Biomedicina de Málaga (IBIMA), Universidad de Málaga, Málaga, Spain.
Mercedes Martín-RufiánDepartamento de Biología Molecular y Bioquímica and Instituto de Investigación de Biomedicina de Málaga (IBIMA), Universidad de Málaga, Málaga, Spain.
Carolina LoboDepartamento de Biología Molecular y Bioquímica and Instituto de Investigación de Biomedicina de Málaga (IBIMA), Universidad de Málaga, Málaga, Spain.
Ana PeñalverDepartamento de Biología Molecular y Bioquímica and Instituto de Investigación de Biomedicina de Málaga (IBIMA), Universidad de Málaga, Málaga, Spain.
María C Gómez-GarcíaDepartamento de Biología Molecular y Bioquímica and Instituto de Investigación de Biomedicina de Málaga (IBIMA), Universidad de Málaga, Málaga, Spain.
Janet Martín-CamposDepartamento de Biología Molecular y Bioquímica and Instituto de Investigación de Biomedicina de Málaga (IBIMA), Universidad de Málaga, Málaga, Spain.
Carolina CardonaDepartamento de Biología Molecular y Bioquímica and Instituto de Investigación de Biomedicina de Málaga (IBIMA), Universidad de Málaga, Málaga, Spain.
Laura CastillaDepartamento de Biología Molecular y Bioquímica and Instituto de Investigación de Biomedicina de Málaga (IBIMA), Universidad de Málaga, Málaga, Spain.
Felipe da Costa SouzaDepartment of Cell and Developmental Biology, Biomedical Sciences Institute, University of São Paulo, São Paulo, Brazil.
Tzuling ChengIDEAYA Biosciences, South San Francisco, CA, USA.
Juan A SeguraDepartamento de Biología Molecular y Bioquímica and Instituto de Investigación de Biomedicina de Málaga (IBIMA), Universidad de Málaga, Málaga, Spain.
Francisco J AlonsoDepartamento de Biología Molecular y Bioquímica and Instituto de Investigación de Biomedicina de Málaga (IBIMA), Universidad de Málaga, Málaga, Spain.
Rui CuriInterdisciplinary Post-Graduate Program in Health Sciences, Cruzeiro do Sul University, São Paulo, Brazil.
Alison ColquhounDepartment of Cell and Developmental Biology, Biomedical Sciences Institute, University of São Paulo, São Paulo, Brazil.
Ralph J DeBerardinisChildren's Medical Center Research Institute, University of Texas Southwestern Medical Center (UTSMC), Dallas, TX, USA.
Javier MárquezDepartamento de Biología Molecular y Bioquímica and Instituto de Investigación de Biomedicina de Málaga (IBIMA), Universidad de Málaga, Málaga, Spain.
José M MatésDepartamento de Biología Molecular y Bioquímica and Instituto de Investigación de Biomedicina de Málaga (IBIMA), Universidad de Málaga, Málaga, Spain. jmates@uma.es.ORCID http://orcid.org/0000-0001-9795-1993
Instituto de Investigación Biomédica de Málaga · ESUniversidade de São Paulo · BRChildren's Medical Center · USIdeaya Biosciences (United States) · USUniversidade Cruzeiro do Sul · BR

Funding

CAPES CAPES/DGU 250/11Ministerio de Ciencia, Innovación y Universidades FPU17/04084Ministerio de Ciencia y Tecnología RTI2018-096866-B-I00
6 · The paper itself

Abstract

backgroundGlutaminase isoenzymes GLS and GLS2 play apparently opposing roles in cancer: GLS acts as an oncoprotein, while GLS2 (GAB isoform) has context specific tumour suppressive activity. Some microRNAs (miRNAs) have been implicated in progression of tumours, including gliomas. The aim was to investigate the effect of GLS and GAB expression on both miRNAs and oxidative status in glioblastoma cells.

methodsMicroarray profiling of miRNA was performed in GLS-silenced LN229 and GAB-transfected T98G human glioblastoma cells and their wild-type counterparts. Results were validated by real-time quantitative RT-PCR. Oxidative status and antioxidant enzymes were determined by spectrophotometric or fluorescence assays in GLS-silenced LN229 and T98G, and GAB-transfected LN229 and T98G.

resultsMiRNA-146a-5p, miRNA-140-3p, miRNA-21-5p, miRNA-1260a, and miRNA-92a-3p were downregulated, and miRNA-1246 was upregulated when GLS was knocked down. MiRNA-140-3p, miRNA-1246, miRNA-1260a, miRNA-21-5p, and miRNA-146a-5p were upregulated when GAB was overexpressed. Oxidative status (lipid peroxidation, protein carbonylation, total antioxidant capacity, and glutathione levels), as well as antioxidant enzymes (catalase, superoxide dismutase, and glutathione reductase) of silenced GLS glioblastoma cells and overexpressed GAB glioblastoma cells significantly changed versus their respective control glioblastoma cells. MiRNA-1246, miRNA-1260a, miRNA-146a-5p, and miRNA-21-5p have been characterized as strong biomarkers of glioblastoma proliferation linked to both GLS silencing and GAB overexpression. Total glutathione is a reliable biomarker of glioblastoma oxidative status steadily associated to both GLS silencing and GAB overexpression.

conclusionsGlutaminase isoenzymes are related to the expression of some miRNAs and may contribute to either tumour progression or suppression through certain miRNA-mediated pathways, proving to be a key tool to switch cancer proliferation and redox status leading to a less malignant phenotype. Accordingly, GLS and GAB expression are especially involved in glutathione-dependent antioxidant defence.

Indexed as

Gene Expression Regulation, NeoplasticOxidative StressCell Line, TumorDown-RegulationGlioblastomaGlutaminaseHumansIsoenzymesMicroRNAsUp-RegulationGLS2 protein, humanGLS protein, humanGlutaminaseIsoenzymesMicroRNAsAntioxidant enzymesCancerGlioblastomaGlutaminasemicroRNAOxidative stress

Identifiers

PMID33610185
PMCPMC7897386
OpenAlexW3131640921

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.