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Tumour endothelial cells in high metastatic tumours promote metastasis via epigenetic dysregulation of biglycan

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Title: Tumour endothelial cells in high metastatic tumours promote metastasis via epigenetic dysregulation of biglycan
Authors: Maishi, Nako Browse this author →KAKEN DB
Ohba, Yusuke Browse this author →KAKEN DB
Akiyama, Kosuke Browse this author →KAKEN DB
Ohga, Noritaka Browse this author →KAKEN DB
Hamada, Jun-ichi Browse this author →KAKEN DB
Nagao-Kitamoto, Hiroko Browse this author
Alam, Mohammad Towfik Browse this author
Yamamoto, Kazuyuki Browse this author
Kawamoto, Taisuke Browse this author
Inoue, Nobuo Browse this author →KAKEN DB
Taketomi, Akinobu Browse this author →KAKEN DB
Shindoh, Masanobu Browse this author →KAKEN DB
Hida, Yasuhiro Browse this author →KAKEN DB
Hida, Kyoko Browse this author →KAKEN DB
Issue Date: 13-Jun-2016
Publisher: Nature Publishing Group
Journal Title: Scientific reports
Volume: 6
Start Page: 28039
Publisher DOI: 10.1038/srep28039
Abstract: Tumour blood vessels are gateways for distant metastasis. Recent studies have revealed that tumour endothelial cells (TECs) demonstrate distinct phenotypes from their normal counterparts. We have demonstrated that features of TECs are different depending on tumour malignancy, suggesting that TECs communicate with surrounding tumour cells. However, the contribution of TECs to metastasis has not been elucidated. Here, we show that TECs actively promote tumour metastasis through a bidirectional interaction between tumour cells and TECs. Co-implantation of TECs isolated from highly metastatic tumours accelerated lung metastases of low metastatic tumours. Biglycan, a small leucine-rich repeat proteoglycan secreted from TECs, activated tumour cell migration via nuclear factor-kappa B and extracellular signal-regulated kinase 1/2. Biglycan expression was upregulated by DNA demethylation in TECs. Collectively, our results demonstrate that TECs are altered in their microenvironment and, in turn, instigate tumour cells to metastasize, which is a novel mechanism for tumour metastasis.
Rights: https://creativecommons.org/licenses/by/4.0/
Type: article
URI: http://hdl.handle.net/2115/62446
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 樋田 京子

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