Evidence map›Paper›PMID 26646448›Full record

ArticleOncotarget2016

NF-Y activates genes of metabolic pathways altered in cancer cells.

Paolo Benatti, Maria Luisa Chiaramonte, Mariangela Lorenzo, John A Hartley, Daniel Hochhauser, Nerina Gnesutta, Roberto Mantovani, Carol Imbriano, Diletta Dolfini

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing 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

41 citing papers in PubMed.

  1. Review
  2. Article
  3. Journal of medicinal chemistry · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Myo-differentiation reporter screen reveals NF-Y as an activator of PAX3-FOXO1 in rhabdomyosarcoma.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. NF-YAl drives EMT in ClaudinCell death & disease · 2023
    Article
  18. NFYAv1 is a Tumor-Promoting Transcript Associated with Poor Prognosis of Hepatocellular Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2023
    Article
  19. Article
  20. Proteasome regulators in pancreatic cancer.World journal of gastrointestinal oncology · 2022
    Review
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

9 authors.

Paolo BenattiDipartimento di Scienze della Vita, Università di Modena e Reggio Emilia, Modena, Italy.
Maria Luisa ChiaramonteDipartimento di Bioscienze, Università degli Studi di Milano, Milano, Italy.
Mariangela LorenzoDipartimento di Bioscienze, Università degli Studi di Milano, Milano, Italy.
John A HartleyCancer Research UK Drug-DNA Interactions Research Group, UCL Cancer Institute, Paul O'Gorman Building, University College London, London, UK.
Daniel HochhauserCancer Research UK Drug-DNA Interactions Research Group, UCL Cancer Institute, Paul O'Gorman Building, University College London, London, UK.
Nerina GnesuttaDipartimento di Bioscienze, Università degli Studi di Milano, Milano, Italy.
Roberto MantovaniDipartimento di Bioscienze, Università degli Studi di Milano, Milano, Italy.
Carol ImbrianoDipartimento di Scienze della Vita, Università di Modena e Reggio Emilia, Modena, Italy.
Diletta DolfiniDipartimento di Bioscienze, Università degli Studi di Milano, Milano, Italy.

Funding

Cancer Research UK 16569Cancer Research UK C2259/A16569
6 · The paper itself

Abstract

The trimeric transcription factor NF-Y binds to the CCAAT box, an element enriched in promoters of genes overexpressed in tumors. Previous studies on the NF-Y regulome identified the general term metabolism as significantly enriched. We dissect here in detail the targeting of metabolic genes by integrating analysis of NF-Y genomic binding and profilings after inactivation of NF-Y subunits in different cell types. NF-Y controls de novo biosynthetic pathways of lipids, teaming up with the master SREBPs regulators. It activates glycolytic genes, but, surprisingly, is neutral or represses mitochondrial respiratory genes. NF-Y targets the SOCG (Serine, One Carbon, Glycine) and Glutamine pathways, as well as genes involved in the biosynthesis of polyamines and purines. Specific cancer-driving nodes are generally under NF-Y control. Altogether, these data delineate a coherent strategy to promote expression of metabolic genes fuelling anaerobic energy production and other anabolic pathways commonly altered in cancer cells.

Indexed as

Gene Expression Regulation, NeoplasticRNA InterferenceCCAAT-Binding FactorCell Line, TumorGene Expression ProfilingHCT116 CellsHeLa CellsHumansImmunoblottingK562 CellsMetabolic Networks and PathwaysModels, GeneticNeoplasmsOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain ReactionCCAAT-Binding FactorNFYA protein, humanNFYB protein, humancancer metabolismglycolysisNF-YSOCG pathwaytranscription

Identifiers

PMID26646448
PMCPMC4811486

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.