Evidence map›Paper›PMID 27792453›Full record

ArticleCell cycle (Georgetown, Tex.)2016

Metformin targets histone acetylation in cancer-prone epithelial cells.

Elisabet Cuyàs, Salvador Fernández-Arroyo, Jorge Joven, Javier A Menendez

Abstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Metformin and Breast Cancer: Molecular Targets.Journal of mammary gland biology and neoplasia · 2019
    Review
  9. Metformin Reshapes the Methylation Profile in Breast and Colorectal Cancer CellsAsian Pacific journal of cancer prevention : APJCP · 2018
    Article
  10. AMPK: An Epigenetic Landscape Modulator.International journal of molecular sciences · 2018
    Review
  11. Review
  12. Mitostemness.Cell cycle (Georgetown, Tex.) · 2018
    Review
  13. Article
  14. Review
  15. Article
  16. 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

4 authors.

Elisabet Cuyàsa ProCURE (Program Against Cancer Therapeutic Resistance), Metabolism & Cancer Group, Catalan Institute of Oncology , Girona , Catalonia , Spain.
Salvador Fernández-Arroyoc Unitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut d'Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, Reus, Spain, The Campus of International Excellence Southern Catalonia , Tarragona , Spain.
Jorge Jovenc Unitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut d'Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, Reus, Spain, The Campus of International Excellence Southern Catalonia , Tarragona , Spain.
Javier A Menendeza ProCURE (Program Against Cancer Therapeutic Resistance), Metabolism & Cancer Group, Catalan Institute of Oncology , Girona , Catalonia , Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The usage of metabolic intermediates as substrates for chromatin-modifying enzymes provides a direct link between the metabolic state of the cell and epigenetics. Because this metabolism-epigenetics axis can regulate not only normal but also diseased states, it is reasonable to suggest that manipulating the epigenome via metabolic interventions may improve the clinical manifestation of age-related diseases including cancer. Using a model of BRCA1 haploinsufficiency-driven accelerated geroncogenesis, we recently tested the hypothesis that: 1.) metabolic rewiring of the mitochondrial biosynthetic nodes that overproduce epigenetic metabolites such as acetyl-CoA should promote cancer-related acetylation of histone H3 marks; 2.) metformin-induced restriction of mitochondrial biosynthetic capacity should manifest in the epigenetic regulation of histone acetylation. We now provide one of the first examples of how metformin-driven metabolic shifts such as reduction of the 2-carbon epigenetic substrate acetyl-CoA is sufficient to correct specific histone H3 acetylation marks in cancer-prone human epithelial cells. The ability of metformin to regulate mitonuclear communication and modulate the epigenetic landscape in genomically unstable pre-cancerous cells might guide the development of new metabolo-epigenetic strategies for cancer prevention and therapy.

Indexed as

AcetylationAcetyl Coenzyme ABRCA1 ProteinCarcinogenesisEpigenesis, GeneticEpithelial CellsGenomic InstabilityHaploinsufficiencyHistonesMetforminModels, BiologicalNeoplasmsAcetyl Coenzyme ABRCA1 ProteinHistonesMetforminBRCA1epigeneticshistone acetylationmetforminmitochondria

Identifiers

PMID27792453
PMCPMC5224457

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.