Expression data in HUVECs treated with siERG, siFLI1, or both

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. 8 samples are uploaded. Human umbilical vein endothelial cells (HUVECs) were treated with siControl, siERG, siFLI1 or siERG+siFLI1 for 3 or 7 days.