Protein N-Homocysteinylation and Colorectal Cancer

Hieronim Jakubowski

doi:10.1016/j.trecan.2018.10.006

Protein N-Homocysteinylation and Colorectal Cancer

Trends Cancer. 2019 Jan;5(1):7-10. doi: 10.1016/j.trecan.2018.10.006. Epub 2018 Nov 13.

Author

Hieronim Jakubowski¹

Affiliation

¹ Department of Microbiology, Biochemistry and Molecular Genetics, Rutgers-New Jersey Medical School, International Center for Public Health, 225 Warren Street, Newark, NJ 07103-3535, USA; Department of Biochemistry and Biotechnology, Poznań University of Life Sciences, Dojazd 11, 60-632 Poznań, Poland. Electronic address: jakubows@rutgers.edu.

PMID: 30616758
DOI: 10.1016/j.trecan.2018.10.006

Abstract

High-fat diet is associated with elevated plasma homocysteine (Hcy), and both are linked to cancer. Although Hcy is not a coded amino acid, proteins do carry Hcy modifications formed via a pathway involving methionyl-tRNA synthetase-catalyzed metabolic conversion of Hcy to Hcy-thiolactone. Hcy-thiolactone then chemically reacts with protein lysine residues, affording KHcy-protein. Recently, Wang et al.[1] (Cell Rep. 2018;25:398-412.e6) showed that this pathway promotes colorectal cancer by impairing DNA damage repair.

Keywords: DNA damage repair; MARS; colorectal cancer; homocysteine editing; posttranslational protein modification.

Publication types

Letter
Research Support, Non-U.S. Gov't

MeSH terms

Colorectal Neoplasms / etiology
Colorectal Neoplasms / metabolism*
DNA Repair
Homocysteine / metabolism*
Humans
Metabolic Networks and Pathways
Protein Processing, Post-Translational*

Substances

Homocysteine