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Số người truy cập: 107,083,999

 A cassaine diterpene alkaloid, 3β-acetyl-nor-erythrophlamide,
suppresses VEGF-induced angiogenesis and tumor growth via
inhibiting eNOS activation
Tác giả hoặc Nhóm tác giả: Nara Tae, Tran Manh Hung, Okwha Kim, Namho Kim, Suhyun Lee, Sunghun
Na, Byung-Sun Min and Jeong-Hyung Lee
Nơi đăng: Oncotarget; Số: Advance online;Từ->đến trang: 1-13;Năm: 2017
Lĩnh vực: Y - Dược; Loại: Bài báo khoa học; Thể loại: Quốc tế
TÓM TẮT
Angiogenesis is one of the hallmarks of cancer, playing an essential role in
tumor growth, invasion, and metastasis. 3β-Acetyl-nor-erythrophlamide (3-ANE),
a cassaine diterpene alkaloid compound from Erythrophleum fordii, exerts various
pharmacological effects, including antitumor activity. However, the effects of 3-ANE
on tumor angiogenesis and its potential molecular mechanism are still unknown.
Here, we demonstrated that 3-ANE inhibited the vascular endothelial growth
factor (VEGF)-mediated proliferation, migration, invasion, and capillary-like tube
formation of human umbilical vascular endothelial cells (HUVECs), without inducing
apoptosis. We also found that 3-ANE blocked angiogenesis in vivo, and suppressed
tumor angiogenesis and human lung adenocarcinoma growth in the xenograft tumor
model. Furthermore, we showed that 3-ANE blocked VEGF-mediated endothelial nitric
oxide synthase (eNOS) phosphorylation, vascular permeability and NO production in
HUVECs, via disrupting the VEGF-induced association of eNOS and heat-shock protein
90 (HSP90). Our studies therefore provide the first evidence that 3-ANE inhibits tumor
angiogenesis by inhibiting the VEGF-mediated eNOS activation and NO production,
and 3-ANE could be a potential candidate in angiogenesis-related disease therapy.
ABSTRACT
Angiogenesis is one of the hallmarks of cancer, playing an essential role in
tumor growth, invasion, and metastasis. 3β-Acetyl-nor-erythrophlamide (3-ANE),
a cassaine diterpene alkaloid compound from Erythrophleum fordii, exerts various
pharmacological effects, including antitumor activity. However, the effects of 3-ANE
on tumor angiogenesis and its potential molecular mechanism are still unknown.
Here, we demonstrated that 3-ANE inhibited the vascular endothelial growth
factor (VEGF)-mediated proliferation, migration, invasion, and capillary-like tube
formation of human umbilical vascular endothelial cells (HUVECs), without inducing
apoptosis. We also found that 3-ANE blocked angiogenesis in vivo, and suppressed
tumor angiogenesis and human lung adenocarcinoma growth in the xenograft tumor
model. Furthermore, we showed that 3-ANE blocked VEGF-mediated endothelial nitric
oxide synthase (eNOS) phosphorylation, vascular permeability and NO production in
HUVECs, via disrupting the VEGF-induced association of eNOS and heat-shock protein
90 (HSP90). Our studies therefore provide the first evidence that 3-ANE inhibits tumor
angiogenesis by inhibiting the VEGF-mediated eNOS activation and NO production,
and 3-ANE could be a potential candidate in angiogenesis-related disease therapy.
[ oncotarget 2017.pdf ]
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