SETDB1 interactions with PELP1 contributes to breast cancer endocrine therapy resistance via Akt activation. SETDB1 interactions with PELP1 contributes to breast cancer endocrine therapy resistance via Akt activation

In this study, we examined the mechanisms by which SETDB1 regulate the cell viability of estrogen receptor (ER) positive breast cancer cells. MCF7 cells were stably transfected with non-targeted shRNA or SETDB1 shRNA via lentiviral transduction. Total RNA was isolated and utilized for RNA-seq analysis. Our results demonstrated that SETDB1 regulates the expression of subsets of genes involved in ER-and Akt-signaling. Overall design: Total RNA from MCF7 control-shRNA and SETDB1-shRNA cells were isolated using RNeasy mini kit (Qiagen). For whole-genome transcriptome profiling, 2 libraries (3 replicates each for knockdown and control) were generated from total RNA from non-targeted shRNA and SETDB1-shRNA transfected MCF7 cells, using a TruSeq Stranded mRNA Library Preparation kit according to the manufacturer’s protocol (Illumina Inc.). Samples were sequenced on the Illumina HiSeq 3000 platform (Illumina Inc.) using the 50 base-pair single-read (50SR) sequencing module.