GEP100-Arf6-AMAP1-Cortactin Pathway Frequently Used in Cancer Invasion Is Activated by VEGFR2 to Promote Angiogenesis

Hashimoto, Ari; Hashimoto, Shigeru; Ando, Ryo; Noda, Kosuke; Ogawa, Eiji; Kotani, Hirokazu; Hirose, Mayumi; Menju, Toshi; Morishige, Masaki; Manabe, Toshiaki; Toda, Yoshinobu; Ishida, Susumu; Sabe, Hisataka

GEP100-Arf6-AMAP1-Cortactin Pathway Frequently Used in Cancer Invasion Is Activated by VEGFR2 to Promote Angiogenesis

Hashimoto, Ari; Hashimoto, Shigeru; Ando, Ryo et al.

PLoS One, 2011, 6(8), e23359

Permalink : https://hdl.handle.net/2115/47068

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アクセス権	open access
URI	https://hdl.handle.net/2115/47068
タイトル	GEP100-Arf6-AMAP1-Cortactin Pathway Frequently Used in Cancer Invasion Is Activated by VEGFR2 to Promote Angiogenesis
著者	Hashimoto, Ari ; Hashimoto, Shigeru ; Ando, Ryo ; Noda, Kosuke ; Ogawa, Eiji ; Kotani, Hirokazu ; Hirose, Mayumi ; Menju, Toshi ; Morishige, Masaki ; Manabe, Toshiaki ; Toda, Yoshinobu ; Ishida, Susumu ; Sabe, Hisataka
著者名 Hashimoto, Ari
著者名 Hashimoto, Shigeru
著者名 Ando, Ryo
著者名 Noda, Kosuke
著者名 Ogawa, Eiji
著者名 Kotani, Hirokazu
著者名 Hirose, Mayumi
著者名 Menju, Toshi
著者名 Morishige, Masaki
著者名 Manabe, Toshiaki
著者名 Toda, Yoshinobu
著者名 Ishida, Susumu
e-Rad_Researcher 40187282 著者名 Sabe, Hisataka
言語	英語
発行日	2011-08-15
出版者	Public Library of Science
収録物名	PLoS One
巻(号)	6(8)
ページ	e23359
抄録	Angiogenesis and cancer invasiveness greatly contribute to cancer malignancy. Arf6 and its effector, AMAP1, are frequently overexpressed in breast cancer, and constitute a central pathway to induce the invasion and metastasis. In this pathway, Arf6 is activated by EGFR via GEP100. Arf6 is highly expressed also in human umbilical vein endothelial cells (HUVECs) and is implicated in angiogenesis. Here, we found that HUVECs also highly express AMAP1, and that vascular endothelial growth factor receptor-2 (VEGFR2) recruits GEP100 to activate Arf6. AMAP1 functions by binding to cortactin in cancer invasion and metastasis. We demonstrate that the same GEP100-Arf6-AMAP1-cortactin pathway is essential for angiogenesis activities, including cell migration and tubular formation, as well as for the enhancement of cell permeability and VE-cadherin endocytosis of VEGF-stimulated HUVECs. Components of this pathway are highly expressed in pathologic angiogenesis, and blocking of this pathway effectively inhibits VEGF- or tumor-induced angiogenesis and choroidal neovascularization. The GEP100-Arf6-AMAP1-cortactin pathway, activated by receptor tyrosine kinases, appears to be common in angiogenesis and cancer invasion and metastasis, and provides their new therapeutic targets.
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	1932-6203
関連情報 (isIdenticalTo)	出版社版DOI https://doi.org/10.1371/journal.pone.0023359