Research Papers:

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 and Diletta Dolfini _

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Oncotarget. 2016; 7:1633-1650. https://doi.org/10.18632/oncotarget.6453

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Paolo Benatti1, Maria Luisa Chiaramonte2, Mariangela Lorenzo2, John A. Hartley3, Daniel Hochhauser3, Nerina Gnesutta2, Roberto Mantovani2, Carol Imbriano1 and Diletta Dolfini2

1 Dipartimento di Scienze della Vita, Università di Modena e Reggio Emilia, Modena, Italy

2 Dipartimento di Bioscienze, Università degli Studi di Milano, Milano, Italy

3 Cancer Research UK Drug-DNA Interactions Research Group, UCL Cancer Institute, Paul O’Gorman Building, University College London, London, UK

Correspondence to:

Diletta Dolfini, email:

Keywords: transcription, cancer metabolism, NF-Y, glycolysis, SOCG pathway

Received: July 14, 2015 Accepted: November 15, 2015 Published: December 03, 2015


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.

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