Evidence map›Paper›PMID 23747254›Full record

ArticleCell metabolism2013

The mitochondrial chaperone TRAP1 promotes neoplastic growth by inhibiting succinate dehydrogenase.

Marco Sciacovelli, Giulia Guzzo, Virginia Morello, Christian Frezza, Liang Zheng, Nazarena Nannini, Fiorella Calabrese, Gabriella Laudiero, Franca Esposito, Matteo Landriscina and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers.

0numbers the graph read from it
0cells of the map it votes in
161citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

161 citing papers in PubMed, 270 citations in OpenAlex.

  1. Article
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  8. TRAP1 and its therapeutic potential.Bioorganic & medicinal chemistry letters · 2025
    Review
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101 more citing papers are in PubMed but not listed here.

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

13 authors at 6 institutions in 2 countries.

Marco SciacovelliCNR Institute of Neuroscience, Department of Biomedical Sciences and Venetian Institute of Molecular Medicine, University of Padova, 35121 Padova, Italy.
Giulia GuzzoCNR Institute of Neuroscience, Department of Biomedical Sciences and Venetian Institute of Molecular Medicine, University of Padova, 35121 Padova, Italy.
Virginia MorelloMolecular Biotechnology Centre, Department of Genetics, Biology and Biochemistry, University of Torino, 10125 Torino, Italy.
Christian FrezzaCancer Research United Kingdom, The Beatson Institute for Cancer Research, Glasgow G61 1BD, UK.
Liang ZhengCancer Research United Kingdom, The Beatson Institute for Cancer Research, Glasgow G61 1BD, UK; Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow G61 1BD, UK.
Nazarena NanniniDepartment of Cardiac, Thoracic and Vascular Sciences, University of Padova, 35121 Padova, Italy.
Fiorella CalabreseDepartment of Cardiac, Thoracic and Vascular Sciences, University of Padova, 35121 Padova, Italy.
Gabriella LaudieroDepartment of Molecular Medicine and Medical Biotechnologies, University of Napoli Federico II, 80131 Napoli, Italy.
Franca EspositoDepartment of Molecular Medicine and Medical Biotechnologies, University of Napoli Federico II, 80131 Napoli, Italy.
Matteo LandriscinaDepartment of Medical and Surgical Sciences, University of Foggia, 71100 Foggia, Italy.
Paola DefilippiMolecular Biotechnology Centre, Department of Genetics, Biology and Biochemistry, University of Torino, 10125 Torino, Italy.
Paolo BernardiCNR Institute of Neuroscience, Department of Biomedical Sciences and Venetian Institute of Molecular Medicine, University of Padova, 35121 Padova, Italy. Electronic address: bernardi@bio.unipd.it.
Andrea RasolaCNR Institute of Neuroscience, Department of Biomedical Sciences and Venetian Institute of Molecular Medicine, University of Padova, 35121 Padova, Italy. Electronic address: rasola@bio.unipd.it.
Veneto Institute of Molecular Medicine · ITCancer Research UK Scotland Institute · GBUniversity of Naples Federico II · ITUniversity of Padua · ITUniversity of Turin · ITUniversity of Foggia · IT

Funding

Cancer Research UKMedical Research Council MC_UU_12022/6Telethon GGP11082
6 · The paper itself

Abstract

We report that the mitochondrial chaperone TRAP1, which is induced in most tumor types, is required for neoplastic growth and confers transforming potential to noncancerous cells. TRAP1 binds to and inhibits succinate dehydrogenase (SDH), the complex II of the respiratory chain. The respiratory downregulation elicited by TRAP1 interaction with SDH promotes tumorigenesis by priming the succinate-dependent stabilization of the proneoplastic transcription factor HIF1α independently of hypoxic conditions. These findings provide a mechanistic clue to explain the switch to aerobic glycolysis of tumors and identify TRAP1 as a promising antineoplastic target.

Indexed as

CarcinogenesisCell Line, TumorCell ProliferationHeLa CellsHSP90 Heat-Shock ProteinsHumansHypoxia-Inducible Factor 1, alpha SubunitMitochondriaNeoplasmsOxygen ConsumptionRNA InterferenceRNA, Small InterferingSuccinate DehydrogenaseHIF1A protein, humanHSP90 Heat-Shock ProteinsHypoxia-Inducible Factor 1, alpha SubunitRNA, Small InterferingSuccinate DehydrogenaseTRAP1 protein, human

Identifiers

PMID23747254
PMCPMC3677096
OpenAlexW2122127456

What OpenQuestion holds

Textmetadata
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.