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)
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