Abstract
Cancer is one of the most important causes of morbidity and mortality worldwide. Tumor cells grow in a complex microenvironment constituted of immune, stromal, and vascular cells that supports growth, angiogenesis, and metastasis. Endothelial cells (ECs) are major components of the vascular microenvironment. These cells have been described for their plasticity and potential to transdifferentiate into mesenchymal cells through a process known as endothelial-to-mesenchymal transition (EndMT). This complex process is controlled by various factors, by which ECs convert into a phenotype characterized by mesenchymal protein expression and motile, contractile morphology. Initially described in normal heart development, EndMT is now identified in several pathologies, and especially in cancer. In this review, we highlight the process of EndMT in the context of cancer and we discuss it as an important adaptive process of the tumor microenvironment that favors tumor growth and dissemination but also resistance to treatment. Thus, we underline targeting of EndMT as a potential therapeutic strategy.
Highlights
The tumor microenvironment (TME) is a complex network of stromal fibroblastic, immune, and endothelial cells (ECs), embedded in a supportive extracellular matrix
This review aims to describe the main features and roles of endothelial-to-mesenchymal transition (EndMT) in cancer and to highlight its importance in shaping a tumor supportive microenvironment that favors tumor growth, metastatic dissemination, and resistance to treatment
Hepatocyte growth factor (HGF) (Huang et al, 2016) and platelet-derived growth factor (PDGF) (Liu T. et al, 2018), two growth factors secreted by tumor cells, appear critical to drive EndMT
Summary
The tumor microenvironment (TME) is a complex network of stromal fibroblastic, immune, and endothelial cells (ECs), embedded in a supportive extracellular matrix. In response to tumor environmental cues, ECs promote the formation of new vessels through proliferation, migration, adhesion, and matrix digestion to support tumor progression and dissemination (Potente et al, 2011) Beside their role in angiogenesis, ECs have been characterized the last decade as capable of an important phenotypic plasticity (Dejana et al, 2017), illustrated by their ability to modify their endothelial phenotype toward a mesenchymal profile. The EndMT process is characterized as a transdifferentiation program where ECs lose their endothelial characteristics and gain mesenchymal features This phenotypic switch is characterized by profound morphological, functional and molecular changes. EndMT has been discovered in tumor specimen of human patients in a number of cancers: colorectal carcinoma (Fan et al, 2018), pancreatic ductal adenocarcinoma (Fan et al, 2019), lung cancer (Choi et al, 2018), or glioblastoma (GBM) (Huang et al, 2016; Table 1)
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