Evidence map›Paper›PMID 29728715›Full record

ReviewCellular and molecular life sciences : CMLS2018

Including the mitochondrial metabolism of L-lactate in cancer metabolic reprogramming.

Lidia de Bari, Anna Atlante

Abstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed.

  1. Article
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  16. Chronic inflammation and long-lasting changes in the gastric mucosa after Helicobacter pylori infection involved in gastric cancer.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Review
  17. Review
  18. Article
  19. Postbiotics, Metabolic Signaling, and Cancer.Molecules (Basel, Switzerland) · 2021
    Review
  20. Article
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

2 authors.

Lidia de BariIstituto di Biomembrane, Bioenergetica e Biotecnologie Molecolari (IBIOM)-CNR, Via G. Amendola 165/A, 70126, Bari, Italy. l.debari@ibiom.cnr.it.ORCID http://orcid.org/0000-0003-2164-5660
Anna AtlanteIstituto di Biomembrane, Bioenergetica e Biotecnologie Molecolari (IBIOM)-CNR, Via G. Amendola 165/A, 70126, Bari, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucose avidity, high glycolysis and L-lactate production, regardless of oxygen availability, are the main traits of cancer metabolic reprogramming. The idea that mitochondria are dysfunctional in cancer, thus causing a glycolysis increase for ATP production and L-lactate accumulation as a dead-end product of glucose catabolism, has oriented cancer research for many years. However, it was shown that mitochondrial metabolism is essential for cancer cell proliferation and tumorigenesis and that L-lactate is a fundamental energy substrate with tumor growth-promoting and signaling capabilities. Nevertheless, the known ability of mitochondria to take up and oxidize L-lactate has remained ignored by cancer research. Beginning with a brief overview of the metabolic changes occurring in cancer, we review the present knowledge of L-lactate formation, transport, and intracellular oxidation and underline the possible role of L-lactate metabolism as energetic, signaling and anabolic support for cancer cell proliferation. These unexplored aspects of cancer biochemistry might be exploited for therapeutic benefit.

Indexed as

Energy MetabolismAdenosine TriphosphateCell ProliferationGlycolysisHumansLactic AcidMitochondriaModels, BiologicalNeoplasmsOxidative PhosphorylationAdenosine TriphosphateLactic AcidAnaplerosisLactate mitochondrial transportOxidative phosphorylationShuttleSignalingTumor

Identifiers

PMID29728715
PMCPMC11105303

What OpenQuestion holds

Textmetadata
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.