ROS enhance angiogenic properties via regulation of NRF2 in tumor endothelial cells

Hojo, Takayuki; Maishi, Nako; Towfik, Alam Mohammad; Akiyama, Kosuke; Ohga, Noritaka; Shindoh, Masanobu; Hida, Yasuhiro; Minowa, Kazuyuki; Fujisawa, Toshiaki; Hida, Kyoko

ROS enhance angiogenic properties via regulation of NRF2 in tumor endothelial cells

Hojo, Takayuki; Maishi, Nako; Towfik, Alam Mohammad et al.

Oncotarget, 2017, 8(28), 45484-45495

Permalink : https://hdl.handle.net/2115/67123

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論文情報

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アクセス権	open access
URI	https://hdl.handle.net/2115/67123
タイトル	ROS enhance angiogenic properties via regulation of NRF2 in tumor endothelial cells
著者	Hojo, Takayuki ; Maishi, Nako ; Towfik, Alam Mohammad ; Akiyama, Kosuke ; Ohga, Noritaka ; Shindoh, Masanobu ; Hida, Yasuhiro ; Minowa, Kazuyuki ; Fujisawa, Toshiaki ; Hida, Kyoko
著者名 Hojo, Takayuki
e-Rad_Researcher 00632423 著者名 Maishi, Nako
著者名 Towfik, Alam Mohammad
e-Rad_Researcher 10609100 著者名 Akiyama, Kosuke
e-Rad_Researcher 40548202 著者名 Ohga, Noritaka
e-Rad_Researcher 20162802 著者名 Shindoh, Masanobu
e-Rad_Researcher 30399919 著者名 Hida, Yasuhiro
著者名 Minowa, Kazuyuki
e-Rad_Researcher 30190028 著者名 Fujisawa, Toshiaki
e-Rad_Researcher 40399952 著者名 Hida, Kyoko
言語	英語
キーワード	tumor angiogenesis
	tumor endothelial cells
	reactive oxygen species
	biglycan
	nuclear factor erythroid 2-related factor 2
発行日	2017-07-11
出版者	Impact Journals
収録物名	Oncotarget
巻(号)	8(28)
ページ	45484-45495
抄録	Reactive oxygen species (ROS) are unstable molecules that activate oxidative stress. Because of the insufficient blood flow in tumors, the tumor microenvironment is often exposed to hypoxic condition and nutrient deprivation, which induces ROS accumulation. We isolated tumor endothelial cells (TECs) and found that they have various abnormalities, although the underlying mechanisms are not fully understood. Here we showed that ROS were accumulated in tumor blood vessels and ROS enhanced TEC migration with upregulation of several angiogenesis related gene expressions. It was also demonstrated that these genes were upregulated by regulation of Nuclear factor erythroid 2-related factor 2 (NRF2). Among these genes, we focused on Biglycan, a small leucine-rich proteoglycan. Inhibition of Toll-like receptors 2 and 4, known BIGLYCAN (BGN) receptors, cancelled the TEC motility stimulated by ROS. ROS inhibited NRF2 expression in TECs but not in NECs, and NRF2 inhibited phosphorylation of SMAD2/3, which activates transcription of BGN. These results indicated that ROS-induced BGN caused the pro-angiogenic phenotype in TECs via NRF2 dysregulation.
資源タイプ	学術雑誌論文
出版タイプ	Version of Record
権利情報	Creative Commons Attribution 3.0 Unported
PISSN	1949-2553
関連情報 (isIdenticalTo)	出版社版DOI https://doi.org/10.18632/oncotarget.17567