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Lysyl oxidase secreted by tumour endothelial cells promotes angiogenesis and metastasis

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Title: Lysyl oxidase secreted by tumour endothelial cells promotes angiogenesis and metastasis
Authors: Osawa, T. Browse this author
Ohga, N. Browse this author →KAKEN DB
Akiyama, K. Browse this author
Hida, Y. Browse this author →KAKEN DB
Kitayama, K. Browse this author →KAKEN DB
Kawamoto, T. Browse this author
Yamamoto, K. Browse this author →KAKEN DB
Maishi, N. Browse this author →KAKEN DB
Kondoh, M. Browse this author →KAKEN DB
Onodera, Y. Browse this author
Fujie, M. Browse this author
Shinohara, N. Browse this author →KAKEN DB
Nonomura, K. Browse this author →KAKEN DB
Shindoh, M. Browse this author →KAKEN DB
Hida, K. Browse this author →KAKEN DB
Keywords: lysyl oxidase
tumour endothelial cells
tumour angiogenesis
Issue Date: 15-Oct-2013
Publisher: NATURE PUBLISHING GROUP
Journal Title: British journal of cancer
Volume: 109
Issue: 8
Start Page: 2237
End Page: 2247
Publisher DOI: 10.1038/bjc.2013.535
PMID: 24045659
Abstract: Background: Molecules that are highly expressed in tumour endothelial cells (TECs) may be candidates for specifically targeting TECs. Using DNA microarray analysis, we found that the lysyl oxidase (LOX) gene was upregulated in TECs compared with its expression in normal endothelial cells (NECs). LOX is an enzyme that enhances invasion and metastasis of tumour cells. However, there are no reports on the function of LOX in isolated TECs. Methods: TECs and NECs were isolated to investigate LOX function in TECs. LOX inhibition of in vivo tumour growth was also assessed using beta-aminopropionitrile (BAPN). Results: LOX expression was higher in TECs than in NECs. LOX knockdown inhibited cell migration and tube formation by TECs, which was associated with decreased phosphorylation of focal adhesion kinase (Tyr 397). Immunostaining showed high LOX expression in human tumour vessels in vivo. Tumour angiogenesis and micrometastasis were inhibited by BAPN in an in vivo tumour model. Conclusion: LOX may be a TEC marker and a possible therapeutic target for novel antiangiogenic therapy.
Rights: http://creativecommons.org/licenses/by-nc-sa/3.0/
Type: article
URI: http://hdl.handle.net/2115/57087
Appears in Collections:歯学院・歯学研究院 (Graduate School of Dental Medicine / Faculty of Dental Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 樋田 京子

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