Evidence mapPaperPMID 36349549Full record

ArticleOpen biology2022

NDUFS3 knockout cancer cells and molecular docking reveal specificity and mode of action of anti-cancer respiratory complex I inhibitors.

Ivana Kurelac, Beatrice Cavina, Manuela Sollazzo, Stefano Miglietta, Agnese Fornasa, Monica De Luise, Maria Iorio, Eleonora Lama, Daniele Traversa, Hamid Razi Nasiri and 5 more

Open access · goldAbstract read
In one paragraph

Article in Open biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

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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

15 authors at 2 institutions in 2 countries.

Ivana KurelacDepartment of Medical and Surgical Sciences (DIMEC), University of Bologna, Bologna, Italy.ORCID 0000-0002-8364-9985
Beatrice CavinaDepartment of Medical and Surgical Sciences (DIMEC), University of Bologna, Bologna, Italy.
Manuela SollazzoDepartment of Pharmacy and Biotechnology (FABIT), University of Bologna, Bologna, Italy.
Stefano MigliettaDepartment of Pharmacy and Biotechnology (FABIT), University of Bologna, Bologna, Italy.
Agnese FornasaDepartment of Pharmacy and Biotechnology (FABIT), University of Bologna, Bologna, Italy.
Monica De LuiseDepartment of Medical and Surgical Sciences (DIMEC), University of Bologna, Bologna, Italy.
Maria IorioDepartment of Medical and Surgical Sciences (DIMEC), University of Bologna, Bologna, Italy.
Eleonora LamaDepartment of Medical and Surgical Sciences (DIMEC), University of Bologna, Bologna, Italy.
Daniele TraversaDepartment of Pharmacy and Biotechnology (FABIT), University of Bologna, Bologna, Italy.ORCID 0000-0002-0522-7381
Hamid Razi NasiriDepartment of Cellular Microbiology, University Hohenheim, Stuttgart, Germany.
Anna GhelliCentre for Applied Biomedical Research (CRBA), University of Bologna, Bologna, Italy.
Francesco MusianiDepartment of Pharmacy and Biotechnology (FABIT), University of Bologna, Bologna, Italy.
Anna Maria PorcelliCentre for Applied Biomedical Research (CRBA), University of Bologna, Bologna, Italy.
Luisa IommariniCentre for Applied Biomedical Research (CRBA), University of Bologna, Bologna, Italy.ORCID 0000-0002-6804-7302
Giuseppe GasparreDepartment of Medical and Surgical Sciences (DIMEC), University of Bologna, Bologna, Italy.
University of Bologna · ITUniversity of Hohenheim · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inhibition of respiratory complex I (CI) is becoming a promising anti-cancer strategy, encouraging the design and the use of inhibitors, whose mechanism of action, efficacy and specificity remain elusive. As CI is a central player of cellular bioenergetics, a finely tuned dosing of targeting drugs is required to avoid side effects. We compared the specificity and mode of action of CI inhibitors metformin, BAY 87-2243 and EVP 4593 using cancer cell models devoid of CI. Here we show that both BAY 87-2243 and EVP 4593 were selective, while the antiproliferative effects of metformin were considerably independent from CI inhibition. Molecular docking predictions indicated that the high efficiency of BAY 87-2243 and EVP 4593 may derive from the tight network of bonds in the quinone binding pocket, although in different sites. Most of the amino acids involved in such interactions are conserved across species and only rarely found mutated in human. Our data make a case for caution when referring to metformin as a CI-targeting compound, and highlight the need for dosage optimization and careful evaluation of molecular interactions between inhibitors and the holoenzyme.

Indexed as

MetforminNeoplasmsElectron Transport Complex IHumansMolecular Docking SimulationNADH DehydrogenasePhenyl EthersQuinazolinesElectron Transport Complex IEVP 4593MetforminNADH DehydrogenaseNDUFS3 protein, humanPhenyl EthersQuinazolinesBAY 87-2243cancer therapycomplex I inhibitorsEVP 4593IACS-010759metforminrespiratory complex I

Identifiers

PMID36349549
PMCPMC9653258
OpenAlexW4308681578

What Socratic 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 Socratic graph.