Genome-wide analysis of ERG- and FLI1-binding in HUVECs, and histone modifications in HUVECs treated with siControl or siERG+siFLI1

Endothelial-to-mesenchymal transition (EndMT) in which endothelial cells lose their characteristics and acquire mesenchymal property has recently been recognized as a driver of disease progression in wide range of pathologies. However, the regulatory mechanism of EndMT has not been fully understood. Here, we found that combined knockdown of two ETS family transcription factors, ERG and FLI1, induced EndMT. Hence, we analyzed functions of ERG and FLI1 using gene expression microarray and ChIP-seq to elucidate the regulatory mechanism of EndMT. 12 samples are uploaded. ChIP was performed for ERG and FLI1 in human umbilical vein endothelial cells (HUVECs); ChIP was performed for H3K4me3 and H3K27Ac in HUVECs treated with siControl or siERG+siFLI1; each sample has two biological replicates.