Evidence map›Paper›PMID 26337086›Full record

ArticleOncotarget2015

Inhibition of glucose-6-phosphate dehydrogenase sensitizes cisplatin-resistant cells to death.

Daniela Catanzaro, Edoardo Gaude, Genny Orso, Carla Giordano, Giulia Guzzo, Andrea Rasola, Eugenio Ragazzi, Laura Caparrotta, Christian Frezza, Monica Montopoli

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

70 citing papers in PubMed, 126 citations in OpenAlex.

  1. Review
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  5. Targeting Lung Cancer Metabolism: Therapeutic Opportunities and Challenges.Advances in experimental medicine and biology · 2026
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10 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

10 authors at 5 institutions in 2 countries.

Daniela CatanzaroDepartment of Pharmaceutical and Pharmacological Sciences, University of Padova, Padova, Italy.
Edoardo GaudeMRC Cancer Unit, University of Cambridge, Hutchison/MRC Research Centre, Cambridge Biomedical Campus, Cambridge, UK.
Genny OrsoIRCCS "E. Medea", Conegliano, Italy.
Carla GiordanoDepartment of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome, Roma, Italy.
Giulia GuzzoDepartment of Biomedical Sciences, University of Padova, Padova, Italy.
Andrea RasolaDepartment of Biomedical Sciences, University of Padova, Padova, Italy.
Eugenio RagazziDepartment of Pharmaceutical and Pharmacological Sciences, University of Padova, Padova, Italy.
Laura CaparrottaDepartment of Pharmaceutical and Pharmacological Sciences, University of Padova, Padova, Italy.
Christian FrezzaMRC Cancer Unit, University of Cambridge, Hutchison/MRC Research Centre, Cambridge Biomedical Campus, Cambridge, UK.
Monica MontopoliDepartment of Pharmaceutical and Pharmacological Sciences, University of Padova, Padova, Italy.
University of Padua · ITHutchison/MRC Research Centre · GBIRCCS Eugenio Medea · ITSapienza University of Rome · ITUniversity of Cambridge · GB

Funding

Medical Research Council MC_UP_1101/3Medical Research Council MC_UU_12022/6
6 · The paper itself

Abstract

The mechanisms of cisplatin resistance, one of the major limitations of current chemotherapy, has only partially been described. We previously demonstrated that cisplatin-resistant ovarian cancer cells (C13), are characterized by reduced mitochondrial activity and higher glucose-dependency when compared to the cisplatin-sensitive counterpart (2008). In this work we further characterized the role of metabolic transformation in cisplatin resistance. By using transmitochondrial hybrids we show that metabolic reprogramming of cisplatin-resistant cell is not caused by inherent mtDNA mutations. We also found that C13 cells not only present an increased glucose-uptake and consumption, but also exhibit increased expression and enzymatic activity of the Pentose Phosphate pathway (PPP) enzyme Glucose-6-Phosphate Dehydrogenase (G6PDH). Moreover, we show that cisplatin-resistant cells are more sensitive to G6PDH inhibition. Even if the metabolomic fingerprint of ovarian cancer cells remains to be further elucidated, these findings indicate that PPP offers innovative potential targets to overcome cisplatin resistance.

Indexed as

Antineoplastic AgentsCell Line, TumorCisplatinDNA, MitochondrialDose-Response Relationship, DrugDrug Resistance, NeoplasmEnergy MetabolismEnzyme InhibitorsFemaleGlucoseGlucosephosphate DehydrogenaseGlutamineHumansMitochondriaOvarian NeoplasmsSignal TransductionAntineoplastic AgentsCisplatinDNA, MitochondrialEnzyme InhibitorsGlucoseGlucosephosphate DehydrogenaseGlutaminecancer metabolismcisplatindrug resistancePPPtransmitochondrial hybrids

Identifiers

PMID26337086
PMCPMC4745784
OpenAlexW2139101652

What OpenQuestion holds

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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.