EMT and EndMT: regulated in similar ways?

• Published in: Journal of biochemistry (Tokyo) Vol. 153; no. 6; pp. 493 - 495
• Main Author: Saito, Akira
• Format: Journal Article
• Language: English
• Published: England 01.06.2013
• Subjects: Animals; Cytokines - metabolism; Endothelial Cells - cytology; Epithelial-Mesenchymal Transition; Humans; Macrophages - metabolism; rho GTP-Binding Proteins - metabolism; Signal Transduction; Smad Proteins - metabolism; Trans-Activators - metabolism; Transforming Growth Factor beta - metabolism; TGF-β; cancer; fibroblast; EMT; EndMT
• ISSN: 0021-924X; 1756-2651; 1756-2651
• DOI: 10.1093/jb/mvt032

Epithelial-mesenchymal transition (EMT) is an evolutionary conserved developmental process, which is evoked during tumour invasion and metastasis. In the tumour microenvironment, a variety of resident and recruited cells participate in tumour progression. Kawata et al. demonstrated an experimental model where proinflammatory cytokines derived from macrophages could enhance EMT of cancer cells. Endothelial-mesenchymal transition (EndMT) is originally observed during heart development, and recent studies suggest its role in pathological settings such as cancer and fibrosis. Mihira et al. demonstrated a line of evidence showing endothelial cell plasticity to undergo EndMT in vitro. Both in EMT and EndMT, transforming growth factor-β played pivotal roles, and multiple downstream mechanisms were used, depending on cell context. These recent works unraveled discrete regulatory networks in mesenchymal transition of epithelial and endothelial cells.