Deacetylation of HP1g enhances multiple myeloma drug resistance through DNA damage repair and liquid-liquid phase separation (RNA-Seq)

Functional crosstalk between histone modifications and chromatin remodeling has emerged as a key regulatory mode of transcriptional control during drug resistance, but the underlying mechanisms are not fully understood. Here we demonstrate that HP1g regulates chromatin dynamic and gene transcription during drug resistance in multiple myeloma. To study the cellular and molecular function of HP1g during bortezomib resistance, we used RNA sequencing (RNA-seq) to generate gene expression profiling under HP1g steady overexpression in LP-1. We identified multiple genes whose expression is significantly affected by HP1g levels. For overexpression condition, LP-1 were infected with HP1g or vector 72h and screened steady the HP1g overexpressed cell lines. Cells were harvested for gene expression profiling including vector and HP1g overexpression cell line. Two replicates were performed per sample.