Evidence map›Paper›PMID 42138716›Full record

ArticleeLife2026

The role of ATP synthase subunit e (ATP5I) in mediating the metabolic and antiproliferative effects of metformin in cancer cells.

Guillaume Lefrançois, Emilie Lavallée, Marie-Camille Rowell, Véronique Bourdeau, Farzaneh Mohebali, Thierry Bertomeu, Ana Maria Duman, Maya Nikolova, Mike Tyers, Simon-Pierre Gravel and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eLife, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Guillaume LefrançoisDepartment of Chemistry, University of Montreal, Montreal, Canada.
Emilie LavalléeFaculté de Pharmacie, University of Montreal, Montreal, Canada.
Marie-Camille RowellDepartment of Biochemistry and Molecular Medicine, CR-CHUM and Montreal Cancer Institute, University of Montreal, Montreal, Canada.
Véronique BourdeauDepartment of Biochemistry and Molecular Medicine, CR-CHUM and Montreal Cancer Institute, University of Montreal, Montreal, Canada.ORCID https://orcid.org/0000-0002-9044-2106
Farzaneh MohebaliDepartment of Chemistry, University of Montreal, Montreal, Canada.
Thierry BertomeuInstitute for Research in Immunology and Cancer, University of Montreal, Montreal, Canada.ORCID https://orcid.org/0000-0002-5313-7057
Ana Maria DumanDepartment of Biochemistry and Molecular Medicine, CR-CHUM and Montreal Cancer Institute, University of Montreal, Montreal, Canada.
Maya NikolovaDepartment of Biochemistry and Molecular Medicine, CR-CHUM and Montreal Cancer Institute, University of Montreal, Montreal, Canada.
Mike TyersInstitute for Research in Immunology and Cancer, University of Montreal, Montreal, Canada.
Simon-Pierre GravelFaculté de Pharmacie, University of Montreal, Montreal, Canada.ORCID https://orcid.org/0000-0001-8411-8054
Andreea R SchmitzerDepartment of Chemistry, University of Montreal, Montreal, Canada.ORCID https://orcid.org/0000-0002-3806-9076
Gerardo FerbeyreDepartment of Biochemistry and Molecular Medicine, CR-CHUM and Montreal Cancer Institute, University of Montreal, Montreal, Canada.ORCID https://orcid.org/0000-0002-2146-618X

Funding

Cancer Research Society 1054571Cancer Research Society 840633Cancer Research Society 935858Cancer Research Society Ganotec/Marc-André Pigeon FundCancer Research Society Operating Grant 2016Natural Sciences and Engineering Research Council of Canada RGPIN-2021-03128Terry Fox Research Institute TFRI Project #1123
6 · The paper itself

Abstract

Here, we identify the subunit e of F₁F₀-ATP synthase (ATP5I) as a target of metformin, a first-in-class antidiabetic biguanide. ATP5I maintains the stability of F₁F₀-ATP synthase dimers, which is crucial for shaping cristae morphology. We demonstrate that ATP5I interacts with a biguanide analogue in vitro, and disabling its expression by CRISPR-Cas9 in pancreatic cancer cells leads to the same phenotype as biguanide-treated cells, including mitochondrial morphology alterations, reduction of the NAD

Indexed as

Antineoplastic AgentsCell ProliferationHypoglycemic AgentsMetforminMitochondrial Proton-Translocating ATPasesCell Line, TumorHumansMitochondriaOxidative PhosphorylationAntineoplastic AgentsHypoglycemic AgentsMetforminMitochondrial Proton-Translocating ATPasesATP5Ibiguanidesbiochemistrychemical biologyF1ATPasehumanmitochondriaNAD metabolismpancreatic cancer

Identifiers

PMID42138716
PMCPMC13179060

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.