Loss of acetylation at Lys16 and trimethylation at Lys20 of histone H4 is a common hallmark of human cancer.

Fraga, Mario F, Ballestar, Esteban, Villar-Garea, Ana, Boix-Chornet, Manuel, Espada, Jesus, Schotta, Gunnar, Bonaldi, Tiziana, Haydon, Claire, Ropero, Santiago, Petrie, Kevin, Iyer, N Gopalakrishna, Pérez-Rosado, Alberto, Calvo, Enrique, Lopez, Juan A, Cano, Amparo, Calasanz, Maria J, Colomer, Dolors, Piris, Miguel Angel, Ahn, Natalie, Imhof, Axel, Caldas, Carlos, Jenuwein, Thomas and Esteller, Manel (2005) Loss of acetylation at Lys16 and trimethylation at Lys20 of histone H4 is a common hallmark of human cancer. Nature genetics, 37 (4). pp. 391-400. ISSN 1061-4036

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Abstract

CpG island hypermethylation and global genomic hypomethylation are common epigenetic features of cancer cells. Less attention has been focused on histone modifications in cancer cells. We characterized post-translational modifications to histone H4 in a comprehensive panel of normal tissues, cancer cell lines and primary tumors. Using immunodetection, high-performance capillary electrophoresis and mass spectrometry, we found that cancer cells had a loss of monoacetylated and trimethylated forms of histone H4. These changes appeared early and accumulated during the tumorigenic process, as we showed in a mouse model of multistage skin carcinogenesis. The losses occurred predominantly at the acetylated Lys16 and trimethylated Lys20 residues of histone H4 and were associated with the hypomethylation of DNA repetitive sequences, a well-known characteristic of cancer cells. Our data suggest that the global loss of monoacetylation and trimethylation of histone H4 is a common hallmark of human tumor cells.

Item Type: Article
Subjects: Sciences > Biomedical Sciences
Sciences > Health Sciences
Divisions: Faculty of Health Sciences and Wellbeing > School of Medicine
Depositing User: Kevin Petrie
Date Deposited: 18 Aug 2020 10:13
Last Modified: 19 Aug 2020 10:13
URI: http://sure.sunderland.ac.uk/id/eprint/12423
ORCID for Kevin Petrie: ORCID iD orcid.org/0000-0002-9805-9152

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