Evidence map›Paper›PMID 33282912›Full record

ArticleFrontiers in molecular biosciences2020

Extracellular Citrate Is a Trojan Horse for Cancer Cells.

Agata Petillo, Vittorio Abruzzese, Prashant Koshal, Angela Ostuni, Faustino Bisaccia

Abstract read
In one paragraph

Article in Frontiers in molecular biosciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Trial
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  10. Antioxidative and Cytoprotective Effects ofFoods (Basel, Switzerland) · 2024
    Article
  11. Article
  12. Article
  13. Review
  14. Engineering metabolism to modulate immunity.Advanced drug delivery reviews · 2024
    Review
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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.

Agata PetilloLaboratory of Cell Biochemistry, Department of Sciences, University of Basilicata, Potenza, Italy.
Vittorio AbruzzeseLaboratory of Cell Biochemistry, Department of Sciences, University of Basilicata, Potenza, Italy.
Prashant KoshalLaboratory of Cell Biochemistry, Department of Sciences, University of Basilicata, Potenza, Italy.
Angela OstuniLaboratory of Cell Biochemistry, Department of Sciences, University of Basilicata, Potenza, Italy.
Faustino BisacciaLaboratory of Cell Biochemistry, Department of Sciences, University of Basilicata, Potenza, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The first intermediate in the mitochondrial tricarboxylic acid (TCA) cycle is citrate, which is essential and acts as a metabolic regulator for glycolysis, TCA cycle, gluconeogenesis, and fatty acid synthesis. Within the cytosol, citrate is cleaved by ATP citrate lyase (ACLY) into oxaloacetate (OAA) and acetyl-CoA; OAA can be used for neoglucogenesis or in the TCA cycle, while acetyl-CoA is the precursor of some biosynthetic processes, including the synthesis of fatty acids. Accumulating evidence suggests that citrate is involved in numerous physiological and pathophysiological processes such as inflammation, insulin secretion, neurological disorders, and cancer. Considering the crucial role of citrate to supply the acetyl-CoA pool for fatty acid synthesis and histone acetylation in tumors, in this study we evaluated the effect of citrate added to the growth medium on lipid deposition and histone H4 acetylation in hepatoma cells (HepG2). At low concentration, citrate increased both histone H4 acetylation and lipid deposition; at high concentration, citrate inhibited both, thus suggesting a crucial role of acetyl-CoA availability, which prompted us to investigate the effect of citrate on ACLY. In HepG2 cells, the expression of ACLY is correlated with histone acetylation, which, in turn, depends on citrate concentration. A decrease in H4 acetylation was also observed when citrate was added at a high concentration to immortalized human hepatic cells, whereas ACLY expression was unaffected, indicating a lack of control by histone acetylation. Considering the strong demand for acetyl-CoA but not for OAA in tumor cells, the exogenous citrate would behave like a trojan horse that carries OAA inside the cells and reduces ACLY expression and cellular metabolism. In addition, this study confirmed the already reported dual role of citrate both as a promoter of cell proliferation (at lower concentrations) and as an anticancer agent (at higher concentrations), providing useful tips on the use of citrate for the treatment of tumors.

Indexed as

ATP citrate lyasecancercitrateepigeneticsHepG2histone acetylationIHH

Identifiers

PMID33282912
PMCPMC7688668

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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.