Endothelial-to-mesenchymal transition in anticancer therapy and normal tissue damage Review


Authors: Choi, K. J.; Nam, J. K.; Kim, J. H.; Choi, S. H.; Lee, Y. J.
Review Title: Endothelial-to-mesenchymal transition in anticancer therapy and normal tissue damage
Abstract: Endothelial-to-mesenchymal transition (EndMT) involves the phenotypic conversion of endothelial-to-mesenchymal cells, and was first discovered in association with embryonic heart development. EndMT can regulate various processes, such as tissue fibrosis and cancer. Recent findings have shown that EndMT is related to resistance to cancer therapy, such as chemotherapy, antiangiogenic therapy, and radiation therapy. Based on the known effects of EndMT on the cardiac toxicity of anticancer therapy and tissue damage of radiation therapy, we propose that EndMT can be targeted as a strategy for overcoming tumor resistance while reducing complications, such as tissue damage. In this review, we discuss EndMT and its roles in damaging cardiac and lung tissues, as well as EndMT-related effects on tumor vasculature and resistance in anticancer therapy. Modulating EndMT in radioresistant tumors and radiation-induced tissue fibrosis can especially increase the efficacy of radiation therapy. In addition, we review the role of hypoxia and reactive oxygen species as the main stimulating factors of tissue damage due to vascular damage and EndMT. We consider drugs that may be clinically useful for regulating EndMT in various diseases. Finally, we argue the importance of EndMT as a therapeutic target in anticancer therapy for reducing tissue damage. © 2020, The Author(s).
Keywords: review; doxorubicin; hypertension; nonhuman; cancer radiotherapy; temozolomide; imatinib; drug inhibition; heart disease; lung cancer; calcitriol; drug resistance; radiation injury; cancer therapy; hypoxia; cell transformation; cardiotoxicity; glioblastoma; diabetes mellitus; blood vessel injury; reactive oxygen metabolite; sepsis; diabetic nephropathy; hydrocortisone; spironolactone; trastuzumab; tumor vascularization; tissue injury; rapamycin; pancreas islet cell tumor; heart muscle fibrosis; tumor microenvironment; radiation induced neoplasm; pulmonary hypertension; lung injury; cinacalcet; proctitis; liraglutide; systemic sclerosis; human; nintedanib; losartan; radiation induced heart disease; 6 [[2 [[4 (2,4 dichlorophenyl) 5 (4 methyl 1h imidazol 2 yl) 2 pyrimidinyl]amino]ethyl]amino]nicotinonitrile; malignant neoplasm; linagliptin; macitentan; vildagliptin; endothelial mesenchymal transition; radiation induced intestinal damage; radiation induced pulmonary fibrosis
Journal Title: Experimental and Molecular Medicine
Volume: 52
Issue: 5
ISSN: 1226-3613
Publisher: Springer Nature  
Date Published: 2020-05-01
Start Page: 781
End Page: 792
Language: English
DOI: 10.1038/s12276-020-0439-4
PUBMED: 32467609
PROVIDER: scopus
PMCID: PMC7272420
DOI/URL:
Notes: Review -- Export Date: 1 July 2020 -- Source: Scopus
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  1. Seo-Hyun Choi
    12 Choi