Evidence map›Paper›PMID 31395464›Full record

ReviewMolecular metabolism2020

Monocarboxylate transporters in cancer.

Valéry L Payen, Erica Mina, Vincent F Van Hée, Paolo E Porporato, Pierre Sonveaux

Open access · goldAbstract readReview
In one paragraph

Review in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 411 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
411citing papers in PubMed, 1 pooled it
18.5field-weighted citation impact, top 1% 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

411 citing papers in PubMed, 1 synthesis or guideline pooled it, 602 citations in OpenAlex.

  1. Pooled it
  2. Recent progress in small molecules targeting the acidic tumor microenvironment.Journal of enzyme inhibition and medicinal chemistry · 2026
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  11. Methylglyoxal AttenuatesInternational journal of molecular sciences · 2026
    Article
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351 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

5 authors at 2 institutions in 2 countries.

Valéry L PayenPole of Pharmacology & Therapeutics, Institut de Recherche Expérimentale et Clinique (IREC), Université catholique de Louvain (UCLouvain), Brussels, Belgium; Pole of Pediatrics, Institut de Recherche Expérimentale et Clinique (IREC), Université catholique de Louvain (UCLouvain), Brussels, Belgium; Louvain Drug Research Institute (LDRI), Université catholique de Louvain (UCLouvain), Brussels, Belgium.
Erica MinaDepartment of Molecular Biotechnology and Health Science, Molecular Biotechnology Center, University of Torino, Torino, Italy.
Vincent F Van HéePole of Pharmacology & Therapeutics, Institut de Recherche Expérimentale et Clinique (IREC), Université catholique de Louvain (UCLouvain), Brussels, Belgium.
Paolo E PorporatoPole of Pharmacology & Therapeutics, Institut de Recherche Expérimentale et Clinique (IREC), Université catholique de Louvain (UCLouvain), Brussels, Belgium; Department of Molecular Biotechnology and Health Science, Molecular Biotechnology Center, University of Torino, Torino, Italy.
Pierre SonveauxPole of Pharmacology & Therapeutics, Institut de Recherche Expérimentale et Clinique (IREC), Université catholique de Louvain (UCLouvain), Brussels, Belgium. Electronic address: pierre.sonveaux@uclouvain.be.
UCLouvain · BEUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumors are highly plastic metabolic entities composed of cancer and host cells that can adopt different metabolic phenotypes. For energy production, cancer cells may use 4 main fuels that are shuttled in 5 different metabolic pathways. Glucose fuels glycolysis that can be coupled to the tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS) in oxidative cancer cells or to lactic fermentation in proliferating and in hypoxic cancer cells. Lipids fuel lipolysis, glutamine fuels glutaminolysis, and lactate fuels the oxidative pathway of lactate, all of which are coupled to the TCA cycle and OXPHOS for energy production. This review focuses on the latter metabolic pathway. SCOPE OF REVIEW: Lactate, which is prominently produced by glycolytic cells in tumors, was only recently recognized as a major fuel for oxidative cancer cells and as a signaling agent. Its exchanges across membranes are gated by monocarboxylate transporters MCT1-4. This review summarizes the current knowledge about MCT structure, regulation and functions in cancer, with a specific focus on lactate metabolism, lactate-induced angiogenesis and MCT-dependent cancer metastasis. It also describes lactate signaling via cell surface lactate receptor GPR81. MAJOR

conclusionsLactate and MCTs, especially MCT1 and MCT4, are important contributors to tumor aggressiveness. Analyses of MCT-deficient (MCT

Indexed as

AnimalsCitric Acid CycleEnergy MetabolismGlucoseHumansLactic AcidMetabolic Networks and PathwaysMiceMice, KnockoutMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersMuscle ProteinsNeoplasmsReceptors, G-Protein-CoupledSymportersGlucoseHCAR1 protein, humanLactic AcidMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersMuscle ProteinsReceptors, G-Protein-CoupledSLC16A4 protein, humanSymportersAngiogenesisCancer metabolismGPR81Metabolic symbiosisMetastasisMonocarboxylate transporters (MCTs)

Identifiers

PMID31395464
PMCPMC7056923
OpenAlexW2964459657

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.