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Updated: May 12, 2026

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
Published on: August 3, 2018
EMT and EndMT: regulated in similar ways?
1Division for Health Service Promotion, University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan. asaitou-tky@umin.ac.jp
Epithelial-mesenchymal transition (EMT) and endothelial-mesenchymal transition (EndMT) are crucial in cancer. Macrophage cytokines can enhance EMT, while transforming growth factor-β influences both EMT and EndMT.
Area of Science:
- Cell biology
- Developmental biology
- Cancer research
Background:
- Epithelial-mesenchymal transition (EMT) is a developmental process implicated in tumor invasion and metastasis.
- The tumor microenvironment involves various cells that promote tumor progression.
- Endothelial-mesenchymal transition (EndMT) is observed in heart development and pathological conditions like cancer.
Purpose of the Study:
- To explore the role of proinflammatory cytokines from macrophages in enhancing cancer cell EMT.
- To investigate the plasticity of endothelial cells in undergoing EndMT.
- To elucidate the distinct regulatory networks governing EMT and EndMT.
Main Methods:
- Experimental modeling of EMT enhancement by macrophage-derived cytokines.
- In vitro studies demonstrating endothelial cell plasticity towards EndMT.
- Comparative analysis of signaling pathways, particularly transforming growth factor-β, in both transitions.
Main Results:
- Proinflammatory cytokines from macrophages can enhance EMT in cancer cells.
- Endothelial cells exhibit plasticity and can undergo EndMT in vitro.
- Transforming growth factor-β plays a pivotal role in both EMT and EndMT, utilizing context-dependent downstream mechanisms.
Conclusions:
- Recent studies reveal discrete regulatory networks for EMT in epithelial cells and EndMT in endothelial cells.
- Understanding these distinct pathways is crucial for targeting cancer invasion and metastasis.
- Macrophage-derived cytokines and TGF-β are key regulators in these mesenchymal transitions.
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