SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFß-independent manner [ATAC-Seq]

SETD2 is one of most frequently mutated genes in renal cell carcinoma. It is generally known as the only histone methyltransferase that catalyze the trimethylation of lysine 36 on histone H3 (H3K36me3). Mutation of this gene and/or loss of its mark have been linked to metastasis and worse patient outcomes in kidney cancer. In this paper, we will examine the mechanism by which SETD2 loss induces epithelial-to-mesenchymal transition (EMT), which is a major pathway that drives invasion and early metastasis in various cancer types. To achieve the goals, we performed several omics analysis including RNA-seq, ChIP-seq and ATAC-seq to characterize how SETD2 deletion alters transcriptome and epigenome. Overall design: Assay for transposase-accessible chromatin DNA-sequencing (ATAC-seq) in SETD2 WT, KO and rescue cells. Each sample is run in duplicates.