Evidence map›Paper›PMID 30318520›Full record

ArticleBritish journal of cancer2018

Mutant p53 blocks SESN1/AMPK/PGC-1α/UCP2 axis increasing mitochondrial O

Marco Cordani, Giovanna Butera, Ilaria Dando, Margalida Torrens-Mas, Elena Butturini, Raffaella Pacchiana, Elisa Oppici, Chiara Cavallini, Sara Gasperini, Nicola Tamassia and 11 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2018. 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 5% 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, 85 citations in OpenAlex.

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  17. [EHHADH is a key gene in fatty acid metabolism pathways in hepatocellular carcinoma: a transcriptomic analysis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
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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 8 institutions in 3 countries.

Marco CordaniDepartment of Neurosciences, Biomedicine and Movement Sciences, Section of Biochemistry, University of Verona, Verona, Italy.
Giovanna ButeraDepartment of Neurosciences, Biomedicine and Movement Sciences, Section of Biochemistry, University of Verona, Verona, Italy.
Ilaria DandoDepartment of Neurosciences, Biomedicine and Movement Sciences, Section of Biochemistry, University of Verona, Verona, Italy.
Margalida Torrens-MasGrupo Multidisciplinar de Oncología Traslacional, Instituto Universitario de Investigación en Ciencias de la Salud (IUNICS), Palma de Mallorca, Illes Balears, Spain.
Elena ButturiniDepartment of Neurosciences, Biomedicine and Movement Sciences, Section of Biochemistry, University of Verona, Verona, Italy.
Raffaella PacchianaDepartment of Neurosciences, Biomedicine and Movement Sciences, Section of Biochemistry, University of Verona, Verona, Italy.
Elisa OppiciDepartment of Neurosciences, Biomedicine and Movement Sciences, Section of Biochemistry, University of Verona, Verona, Italy.
Chiara CavalliniResearch Center LURM (Interdepartmental Laboratory of Medical Research), University of Verona, Verona, Italy.
Sara GasperiniDepartment of Medicine, Section of General Pathology, University of Verona, Verona, Italy.
Nicola TamassiaDepartment of Medicine, Section of General Pathology, University of Verona, Verona, Italy.
Mercedes Nadal-SerranoVall d'Hebron Institut d'Oncologia (VHIO), Barcelona, Spain.
Michela CoanDivision of Molecular Oncology, Department of Translational Research, CRO National Cancer Institute Aviano, Aviano, Italy.
Davide RossiHematology, Oncology Institute of Southern Switzerland, Bellinzona, Switzerland.
Gianluca GaidanoDivision of Hematology, Department of Translational Medicine, University of Eastern Piedmont, Novara, Italy.
Michele CaragliaDepartment of Biochemistry, Biophysics and General Pathology, University of Campania "L. Vanvitelli", Naples, Italy.
Sofia MariottoDepartment of Neurosciences, Biomedicine and Movement Sciences, Section of Biochemistry, University of Verona, Verona, Italy.
Riccardo SpizzoDivision of Molecular Oncology, Department of Translational Research, CRO National Cancer Institute Aviano, Aviano, Italy.
Pilar RocaGrupo Multidisciplinar de Oncología Traslacional, Instituto Universitario de Investigación en Ciencias de la Salud (IUNICS), Palma de Mallorca, Illes Balears, Spain.
Jordi OliverGrupo Multidisciplinar de Oncología Traslacional, Instituto Universitario de Investigación en Ciencias de la Salud (IUNICS), Palma de Mallorca, Illes Balears, Spain.
Maria Teresa ScupoliResearch Center LURM (Interdepartmental Laboratory of Medical Research), University of Verona, Verona, Italy.
Massimo DonadelliDepartment of Neurosciences, Biomedicine and Movement Sciences, Section of Biochemistry, University of Verona, Verona, Italy. massimo.donadelli@univr.it.
University of Verona · ITResearch Institute of Health Sciences · ESCentro di Riferimento Oncologico · ITInstitute of Oncology Research · CHInstituto de Investigaciones Biomédicas Sols-Morreale · ESUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITUniversity of Campania "Luigi Vanvitelli" · ITVall d'Hebron Institut de Recerca · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe TP53 tumor suppressor gene is the most frequently altered gene in tumors and mutant p53 gain-of-function isoforms actively promote cancer malignancy.

methodsA panel of wild-type and mutant p53 cancer cell lines of different tissues, including pancreas, breast, skin, and lung were used, as well as chronic lymphocytic leukemia (CLL) patients with different TP53 gene status. The effects of mutant p53 were evaluated by confocal microscopy, reactive oxygen species production assay, immunoblotting, and quantitative reverse transcription polymerase chain reaction after cellular transfection.

resultsWe demonstrate that oncogenic mutant p53 isoforms are able to inhibit SESN1 expression and consequently the amount of SESN1/AMPK complex, resulting in the downregulation of the AMPK/PGC-1α/UCP2 axis and mitochondrial O

conclusionsThe inhibition of the SESN1/AMPK/PGC-1α/UCP2 axis contributes to the pro-oxidant and oncogenic effects of mutant p53, suggesting pro-oxidant drugs as a therapeutic approach for cancer patients bearing mutant TP53 gene.

Indexed as

AcetylcysteineAdultAgedAged, 80 and overAMP-Activated Protein KinasesCell Line, TumorFemaleFree Radical ScavengersHeat-Shock ProteinsHumansMaleMCF-7 CellsMiddle AgedMitochondriaNeoplasmsOxygenAcetylcysteineAMP-Activated Protein KinasesFree Radical ScavengersHeat-Shock ProteinsOxygenPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanReactive Oxygen SpeciesSESN1 protein, humanSestrinsTP53 protein, humanTumor Suppressor Protein p53UCP2 protein, humanUncoupling Protein 2

Identifiers

PMID30318520
PMCPMC6203762
OpenAlexW2897649145

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.