Evidence map›Paper›PMID 32681016›Full record

ArticleNature communications2020

Coordinate β-adrenergic inhibition of mitochondrial activity and angiogenesis arrest tumor growth.

Cristina Nuevo-Tapioles, Fulvio Santacatterina, Konstantinos Stamatakis, Cristina Núñez de Arenas, Marta Gómez de Cedrón, Laura Formentini, José M Cuezva

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

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9 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

7 authors at 3 institutions in 1 country.

Cristina Nuevo-TapiolesDepartamento de Biología Molecular, Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid (CSIC-UAM), Madrid, Spain.ORCID http://orcid.org/0000-0001-5809-2030
Fulvio SantacatterinaDepartamento de Biología Molecular, Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid (CSIC-UAM), Madrid, Spain.ORCID http://orcid.org/0000-0002-4831-5402
Konstantinos StamatakisDepartamento de Biología Molecular, Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid (CSIC-UAM), Madrid, Spain.ORCID http://orcid.org/0000-0001-9934-3502
Cristina Núñez de ArenasDepartamento de Biología Molecular, Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid (CSIC-UAM), Madrid, Spain.
Marta Gómez de CedrónInstituto Madrileño de Estudios Avanzados (IMDEA) Food Institute, Universidad Autónoma de Madrid, 28049, Madrid, Spain.ORCID http://orcid.org/0000-0002-0894-970X
Laura FormentiniDepartamento de Biología Molecular, Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid (CSIC-UAM), Madrid, Spain.ORCID http://orcid.org/0000-0001-5641-821X
José M CuezvaDepartamento de Biología Molecular, Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid (CSIC-UAM), Madrid, Spain. jmcuezva@cbm.csic.es.ORCID http://orcid.org/0000-0003-1118-248X
Consejo Superior de Investigaciones Científicas · ESInstituto de Salud Carlos III · ESMadrid Institute for Advanced Studies · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial metabolism has emerged as a promising target against the mechanisms of tumor growth. Herein, we have screened an FDA-approved library to identify drugs that inhibit mitochondrial respiration. The β1-blocker nebivolol specifically hinders oxidative phosphorylation in cancer cells by concertedly inhibiting Complex I and ATP synthase activities. Complex I inhibition is mediated by interfering the phosphorylation of NDUFS7. Inhibition of the ATP synthase is exerted by the overexpression and binding of the ATPase Inhibitory Factor 1 (IF1) to the enzyme. Remarkably, nebivolol also arrests tumor angiogenesis by arresting endothelial cell proliferation. Altogether, targeting mitochondria and angiogenesis triggers a metabolic and oxidative stress crisis that restricts the growth of colon and breast carcinomas. Nebivolol holds great promise to be repurposed for the treatment of cancer patients.

Indexed as

Adrenergic AntagonistsAngiogenesis Inducing AgentsATPase Inhibitory ProteinBreast NeoplasmsCell Line, TumorCell ProliferationColonic NeoplasmsFemaleHumansMaleMitochondriaMitochondrial Proton-Translocating ATPasesNADH DehydrogenaseNebivololOxidative PhosphorylationProteinsAdrenergic AntagonistsAngiogenesis Inducing AgentsATPase Inhibitory ProteinMitochondrial Proton-Translocating ATPasesNADH DehydrogenaseNDUFS7 protein, humanNebivololProteins

Identifiers

PMID32681016
PMCPMC7368041
OpenAlexW3043495494

What OpenQuestion 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 OpenQuestion graph.