Evidence map›Paper›PMID 41617686›Full record

ArticleCell death & disease2026

Honokiol blocks tumor development and metastasis through mitochondrion-targeted effects.

Martina Grandi, Francesco Boldrin, Giovanni Risato, Silvia Grillini, Natascia Tiso, Francesco Argenton, Emanuela Leonardi, Silvio Tosatto, Giancarlo Solaini, Alessandra Baracca and 1 more

Abstract read
In one paragraph

Article in Cell death & disease, 2026. 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. Review
  2. Review
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

11 authors.

Martina GrandiDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, I-40126, Italy.
Francesco BoldrinDepartment of Biology, University of Padova, Padua, I-35121, Italy.ORCID http://orcid.org/0000-0002-0234-2587
Giovanni RisatoDepartment of Biology, University of Padova, Padua, I-35121, Italy.ORCID http://orcid.org/0000-0003-0651-7409
Silvia GrilliniDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, I-40126, Italy.
Natascia TisoDepartment of Biology, University of Padova, Padua, I-35121, Italy.ORCID http://orcid.org/0000-0002-5444-9853
Francesco ArgentonDepartment of Biology, University of Padova, Padua, I-35121, Italy.ORCID http://orcid.org/0000-0002-0803-8236
Emanuela LeonardiDepartment of Biomedical Sciences, University of Padova, Padua, I-35121, Italy.ORCID http://orcid.org/0000-0001-8486-8461
Silvio TosattoDepartment of Biomedical Sciences, University of Padova, Padua, I-35121, Italy.ORCID http://orcid.org/0000-0003-4525-7793
Giancarlo SolainiDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, I-40126, Italy.
Alessandra BaraccaDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, I-40126, Italy.
Valentina GiorgioDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, I-40126, Italy. valentina.giorgio4@unibo.it.ORCID http://orcid.org/0000-0002-4229-3054

Funding

Associazione Italiana per la Ricerca sul Cancro (Italian Association for Cancer Research) MFAG 2017 - ID. 20316Ministero dell'Istruzione, dell'Università e della Ricerca (Ministry of Education, University and Research) PRIN 2017 - ID. 201789LFKBMinistero dell'Istruzione, dell'Università e della Ricerca (Ministry of Education, University and Research) PRIN 2022- ID. 2022XTSLAP
6 · The paper itself

Abstract

IF1 is the natural inhibitor of the mitochondrial ATP synthase during hydrolytic activity. It has been found to be overexpressed in many tumors, where it acts as a pro-oncogenic protein. During oxidative phosphorylation, IF1 binds to a novel site on the OSCP subunit of ATP synthase and promotes tumorigenesis by protecting cancer cells from permeability transition pore (PTP)-dependent apoptosis. In this work, honokiol, a biphenolic compound, showed binding affinity for two sites on the OSCP subunit, as predicted by molecular docking analysis. It was shown to be effective in disrupting the IF1-OSCP interaction and sensitizing cancer cells to apoptosis. In vivo, xenografts of zebrafish injected with IF1-expressing HeLa cells showed tumor development. The same xenografts, treated with honokiol, showed a significant reduction in tumor mass, similar to untreated fish injected with IF1 KO HeLa cells. In vitro, honokiol inhibits colony formation in soft agar of IF1-expressing HeLa cells by promoting the PTP opening and cell death, without any effect on cell proliferation. Interestingly, honokiol was shown to block metastasis in fish xenografts and migration in a wound healing assay, by promoting mitochondrial swelling in both control and IF1 KO cell lines, when cells are moving to close the scratch area. In conclusion, honokiol appears to be a promising anti-cancer compound, with pro-apoptotic properties through the displacement of IF1 from the OSCP subunit of ATP synthase, and anti-metastatic effects that are due to mitochondrial PTP opening.

Indexed as

Antineoplastic Agents, PhytogenicBiphenyl CompoundsLignansMitochondriaAllyl CompoundsAnimalsApoptosisCell MovementCell ProliferationHeLa CellsHumansMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMitochondrial Proton-Translocating ATPasesMolecular Docking SimulationNeoplasm MetastasisAllyl CompoundsAntineoplastic Agents, PhytogenicBiphenyl CompoundshonokiolLignansMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMitochondrial Proton-Translocating ATPasesPhenols

Identifiers

PMID41617686
PMCPMC12877151

What OpenQuestion holds

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Registered trials

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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.