Downregulation of ERG and FLI1 expression in endothelial cells triggers endothelial-to-mesenchymal transition.

ABSTRACT: Endothelial cell (EC) plasticity in pathological settings has recently been recognized as a driver of disease progression. Endothelial-to-mesenchymal transition (EndMT), in which ECs acquire mesenchymal properties, has been described for a wide range of pathologies, including cancer. However, the mechanism regulating EndMT in the tumor microenvironment and the contribution of EndMT in tumor progression are not fully understood. Here, we found that combined knockdown of two ETS family transcription factors, ERG and FLI1, induces EndMT coupled with dynamic epigenetic changes in ECs. Genome-wide analyses revealed that ERG and FLI1 are critical transcriptional activators for EC-specific genes, among which microRNA-126 partially contributes to blocking the induction of EndMT. Moreover, we demon

SUBMITTER: Nagai N 

PROVIDER: S-EPMC6291168 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature