Evidence map›Paper›PMID 39288141›Full record

ArticlePloS one2024

Repurposing auranofin and meclofenamic acid as energy-metabolism inhibitors and anti-cancer drugs.

Sara Rodríguez-Enríquez, Diana Xochiquetzal Robledo-Cadena, Silvia Cecilia Pacheco-Velázquez, Jorge Luis Vargas-Navarro, Joaquín Alberto Padilla-Flores, Tuuli Kaambre, Rafael Moreno-Sánchez

Abstract read
In one paragraph

Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Current clinical applications and future developments of platinum-based anticancer drugs.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026
    Review
  2. Article
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

7 authors.

Sara Rodríguez-EnríquezLaboratorio de Control Metabólico, Carrera de Médico Cirujano de la Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Tlalnepantla, México.ORCID 0000-0002-0822-1233
Diana Xochiquetzal Robledo-CadenaDepartamento de Bioquímica, Instituto Nacional de Cardiología Ignacio Chávez, Ciudad de México, México.ORCID 0000-0002-7287-938X
Silvia Cecilia Pacheco-VelázquezCenter for Preventive Cardiology, Knight Cardiovascular Institute, Oregon Health & Science University, Portland, Oregon, United States of America.
Jorge Luis Vargas-NavarroLaboratorio de Control Metabólico, Carrera de Médico Cirujano de la Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Tlalnepantla, México.
Joaquín Alberto Padilla-FloresLaboratorio de Control Metabólico, Carrera de Médico Cirujano de la Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Tlalnepantla, México.ORCID 0000-0001-9032-4356
Tuuli KaambreLaboratory of Chemical Biology, National Institute of Chemical Physics and Biophysics, Tallinn, Estonia.
Rafael Moreno-SánchezLaboratorio de Control Metabólico, Carrera de Biología de la Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Tlalnepantla, México.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveCytotoxicity of the antirheumatic drug auranofin (Aur) and the non-steroidal anti-inflammatory drug meclofenamic acid (MA) on several cancer cell lines and isolated mitochondria was examined to assess whether these drugs behave as oxidative phosphorylation inhibitors.

methodsThe effect of Aur or MA for 24 h was assayed on metastatic cancer and non-cancer cell proliferation, energy metabolism, mitophagy and metastasis; as well as on oxygen consumption rates of cancer and non-cancer mitochondria.

resultsAur doses in the low micromolar range were required to decrease proliferation of metastatic HeLa and MDA-MB-231 cells, whereas one or two orders of magnitude higher levels were required to affect proliferation of non-cancer cells. MA doses required to affect cancer cell growth were one order of magnitude higher than those of Aur. At the same doses, Aur impaired oxidative phosphorylation in isolated mitochondria and intact cells through mitophagy induction, as well as glycolysis. Consequently, cell migration and invasiveness were severely affected. The combination of Aur with very low cisplatin concentrations promoted that the effects on cellular functions were potentiated.

conclusionAur surges as a highly promising anticancer drug, suggesting that efforts to establish this drug in the clinical treatment protocols are warranted and worthy to undertake.

Indexed as

Antineoplastic AgentsAuranofinCell ProliferationDrug RepositioningEnergy MetabolismMeclofenamic AcidMitochondriaOxidative PhosphorylationCell Line, TumorCell MovementGlycolysisHeLa CellsHumansMitophagyOxygen ConsumptionAntineoplastic AgentsAuranofinMeclofenamic Acid

Identifiers

PMID39288141
PMCPMC11407620

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.