Genome-wide chromatin accessibility, DNA methylation and gene expression analysis of histone deacetylase inhibition in triple-negative breast cancer

Matias A Bustos; Matthew P Salomon; Nellie Nelson; Sandy C Hsu; Maggie L DiNome; Dave S B Hoon; Diego M Marzese

doi:10.1016/j.gdata.2017.01.002

Genome-wide chromatin accessibility, DNA methylation and gene expression analysis of histone deacetylase inhibition in triple-negative breast cancer

Genom Data. 2017 Feb 14:12:14-16. doi: 10.1016/j.gdata.2017.01.002. eCollection 2017 Jun.

Authors

Matias A Bustos¹, Matthew P Salomon¹, Nellie Nelson², Sandy C Hsu², Maggie L DiNome³, Dave S B Hoon⁴, Diego M Marzese¹

Affiliations

¹ Department of Translational Molecular Medicine, John Wayne Cancer Institute at Providence Saint John's Health Center, Santa Monica, CA 90404, USA.
² Sequencing Center, John Wayne Cancer Institute at Providence Saint John's Health Center, Santa Monica, CA 90404, USA.
³ Department of Surgery, David Geffen School of Medicine, University of California Los Angeles (UCLA), CA, USA.
⁴ Department of Translational Molecular Medicine, John Wayne Cancer Institute at Providence Saint John's Health Center, Santa Monica, CA 90404, USA; Sequencing Center, John Wayne Cancer Institute at Providence Saint John's Health Center, Santa Monica, CA 90404, USA.

Abstract

Triple-negative breast cancer (TNBC), especially the subset with a basal phenotype, represents the most aggressive subtype of breast cancer. Unlike other solid tumors, TNBCs harbor a low number of driver mutations. Conversely, we and others have demonstrated a significant impact of epigenetic alterations, including DNA methylation and histone post-translational modifications, affecting TNBCs. Due to the promising results in pre-clinical studies, histone deacetylase inhibitors (HDACi) are currently being tested in several clinical trials for breast cancer and other solid tumors. However, the genome-wide epigenetic and transcriptomic implications of HDAC inhibition are still poorly understood. Here, we provide detailed information about the design of a multi-platform dataset that describes the epigenomic and transcriptomic effects of HDACi. This dataset includes genome-wide chromatin accessibility (assessed by ATAC-Sequencing), DNA methylation (assessed by Illumina HM450K BeadChip) and gene expression (assessed by RNA-Sequencing) analyses before and after HDACi treatment of HCC1806 and MDA-MB-231, two human TNBC cell lines with basal-like phenotype.