Nature Communications (Apr 2020)
Selective inhibition of cancer cell self-renewal through a Quisinostat-histone H1.0 axis
- Cristina Morales Torres,
- Mary Y. Wu,
- Sebastijan Hobor,
- Elanor N. Wainwright,
- Matthew J. Martin,
- Harshil Patel,
- William Grey,
- Eva Grönroos,
- Steven Howell,
- Joana Carvalho,
- Ambrosius P. Snijders,
- Michael Bustin,
- Dominique Bonnet,
- Paul D. Smith,
- Charles Swanton,
- Michael Howell,
- Paola Scaffidi
Affiliations
- Cristina Morales Torres
- Cancer Epigenetics Laboratory, Francis Crick Institute
- Mary Y. Wu
- High-Throughput Screening, Francis Crick Institute
- Sebastijan Hobor
- Cancer Evolution and Genome Instability Laboratory, Francis Crick Institute
- Elanor N. Wainwright
- Cancer Epigenetics Laboratory, Francis Crick Institute
- Matthew J. Martin
- Oncology R&D, AstraZeneca
- Harshil Patel
- Bioinformatics and Biostatistics, Francis Crick Institute
- William Grey
- Haematopoietic Stem Cell Laboratory, Francis Crick Institute
- Eva Grönroos
- Cancer Evolution and Genome Instability Laboratory, Francis Crick Institute
- Steven Howell
- Proteomics, Francis Crick Institute
- Joana Carvalho
- Experimental Histopathology, Francis Crick Institute
- Ambrosius P. Snijders
- Proteomics, Francis Crick Institute
- Michael Bustin
- Center for Cancer Research, National Cancer Institute, National Institutes of Health
- Dominique Bonnet
- Haematopoietic Stem Cell Laboratory, Francis Crick Institute
- Paul D. Smith
- Oncology R&D, AstraZeneca
- Charles Swanton
- Cancer Evolution and Genome Instability Laboratory, Francis Crick Institute
- Michael Howell
- High-Throughput Screening, Francis Crick Institute
- Paola Scaffidi
- Cancer Epigenetics Laboratory, Francis Crick Institute
- DOI
- https://doi.org/10.1038/s41467-020-15615-z
- Journal volume & issue
-
Vol. 11,
no. 1
pp. 1 – 15
Abstract
Targeting self-renewing cancer cells without deleterious side effects in normal tissues has proven challenging. Here, the authors show that the well-tolerated HDAC inhibitor Quisinostat safely inhibits tumor maintenance and disease relapse by restoring high levels of histone H1.0.
