Project description:Subpopulations of highly tumorigenic, drug resistant cancer stem-like cells play a key role in cancer recurrence and progression. Surprisingly, these aggressive cells can arise repeatedly de novo from bulk tumor cells independently of mutational events. We investigated whether transition to and from a cancer stem-like state is associated with epigenetic alterations, such as DNA methylation and chromatin accessibility. By Hoechst dye staining and FACS analysis, side population (SP) and non-side population cells were sorted from J82 cells. AcceSssIble assay by Infinium EPIC BeadArray platform was used to identify potential epigenetic driver genes in the process of SP /NSP phenotype plasticity. Genes with differential accessible promoter regions were overlapped with genes differentially expressed by HuEx array analysis. Oncomine and Basespace were adopted to explore the clinical relevance of the target genes.