CSB ablation induced apoptosis is mediated by Increased Endoplasmic Reticulum Stress Response: a gene expression study

The DNA repair protein, Cockayne syndrome group B (CSB), has been recently identified as a promising anticancer target. Suppression, by antisense technology, of this protein causes devastating effects on tumor cells viability, through a massive induction of apoptosis, while being non-toxic to non-transformed cells. To gain insights into the mechanisms underlying the pro-apoptotic effects observed after CSB ablation, global gene expression patterns were determined, to identify genes that were significantly differentially regulated as a function of CSB expression. The one-color Agilent microarray platform was used. The study revealed that response to endoplasmic reticulum stress and response to unfolded proteins were ranked top amongst the cellular processes affected by CSB suppression. A total of n=16 samples were processed: 4 experimental groups, 2 time points (6 and 12 h after transfection) and 2 biological replicates for each experimental point(time+group). The 4 experimental groups (one test and three controls) are: cells incubated with antisense oligonucleotides specifically inducing CSB mRNA degradation (ASO), mock treated cells (CTRL), transfection reagents alone (OLF) and cells treated with sense oligonucleotides (SO).