Increased formate overflow is a hallmark of oxidative cancer

Johannes Meiser, Anne Schuster, Matthias Pietzke, Johan Vande Voorde, Dimitris Athineos, Kristell Oizel, Guillermo Burgos-Barragan, Niek Wit, Sandeep Dhayade, Jennifer P. Morton, Emmanuel Dornier, David Sumpton, Gillian M. Mackay, Karen Blyth, Ketan J. Patel, Simone P. Niclou and Alexei Vazquez ()
Additional contact information
Johannes Meiser: Cancer Research UK Beatson Institute
Anne Schuster: Luxembourg Institute of Health
Matthias Pietzke: Cancer Research UK Beatson Institute
Johan Vande Voorde: Cancer Research UK Beatson Institute
Dimitris Athineos: Cancer Research UK Beatson Institute
Kristell Oizel: Cancer Research UK Beatson Institute
Guillermo Burgos-Barragan: MRC Laboratory of Molecular Biology
Niek Wit: MRC Laboratory of Molecular Biology
Sandeep Dhayade: Cancer Research UK Beatson Institute
Jennifer P. Morton: Cancer Research UK Beatson Institute
Emmanuel Dornier: Cancer Research UK Beatson Institute
David Sumpton: Cancer Research UK Beatson Institute
Gillian M. Mackay: Cancer Research UK Beatson Institute
Karen Blyth: Cancer Research UK Beatson Institute
Ketan J. Patel: MRC Laboratory of Molecular Biology
Simone P. Niclou: Luxembourg Institute of Health
Alexei Vazquez: Cancer Research UK Beatson Institute

Nature Communications, 2018, vol. 9, issue 1, 1-12

Abstract: Abstract Formate overflow coupled to mitochondrial oxidative metabolism\ has been observed in cancer cell lines, but whether that takes place in the tumor microenvironment is not known. Here we report the observation of serine catabolism to formate in normal murine tissues, with a relative rate correlating with serine levels and the tissue oxidative state. Yet, serine catabolism to formate is increased in the transformed tissue of in vivo models of intestinal adenomas and mammary carcinomas. The increased serine catabolism to formate is associated with increased serum formate levels. Finally, we show that inhibition of formate production by genetic interference reduces cancer cell invasion and this phenotype can be rescued by exogenous formate. We conclude that increased formate overflow is a hallmark of oxidative cancers and that high formate levels promote invasion via a yet unknown mechanism.

Date: 2018
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-018-03777-w Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-03777-w

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-018-03777-w

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().