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Carcinogenesis Advance Access originally published online on April 21, 2005
Carcinogenesis 2005 26(8):1436-1445; doi:10.1093/carcin/bgi097
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Carcinogenesis vol.26 no.8 © Oxford University Press 2005; all rights reserved.

Penta-O-galloyl-beta-D-glucose suppresses tumor growth via inhibition of angiogenesis and stimulation of apoptosis: roles of cyclooxygenase-2 and mitogen-activated protein kinase pathways

Jeong-Eun Huh, Eun-Ok Lee, Min-Seok Kim 1, Kyung-Sun Kang 2, Cheol-Ho Kim 3, Bae-Cheon Cha 4, Young-Joon Surh 5 and Sung-Hoon Kim *

Graduate School of East-West Medical Science, KyungHee University, Yongin 449-701, 1 Department of Molecular Biology, University of Wisconsin, Madison, Wisconsin 53706, USA, 2 Department of Veterinary Public Health, College of Veterinary Medicine, Seoul 151-742, 3 Department of Biochemistry and Molecular Biology, College of Oriental Medicine, Dongguk University, Kyungju 780-714, 4 Department of Applied Animal Sciences, College of Life Sciences and Natural Resources, Sangji University, Wonju 220-702 and 5 College of Pharmacy, Seoul National University, Seoul 151-742, Republic of Korea

* To whom correspondence should be addressed Email: sungkim7{at}khu.ac.kr

Recent studies have revealed that 1,2,3,4,6-penta-O-galloyl-beta-D-glucose (PGG) has anti-tumorigenic activity in vitro. In the present work, we evaluated the in vitro and in vivo antiangiogenic and antitumor activities of PGG and examined its molecular mechanisms. PGG significantly inhibited the proliferation and tube formation in basic fibroblast growth factor (bFGF)-treated human umbilical vein endothelial cells (HUVECs) at non-cytotoxic concentrations. PGG effectively disrupted the bFGF-induced neo-vascularization in chick chorioallantoic membrane (CAM) and in Matrigel plugs in the mice. When mice were intraperitoneally injected, PGG also significantly inhibited tumor angiogenesis induced by Lewis lung carcinoma (LLC) and the growth of LLC by 57 and 91% of control tumor weight at 4 and 20 mg/kg, respectively. Immunohistochemical analysis revealed decreased microvessel density, decreased expression of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF), reduced tumor cell proliferation and increased tumor cell apoptosis. Similarly, PGG significantly attenuated the expression of COX-2 and VEGF and reduced the secretion of VEGF and prostaglandin E2 in bFGF-treated HUVECs. Furthermore, the COX-2 inhibitor NS398 significantly inhibited tube formation and neo-vascularization in CAM, supporting the role of COX-2 in PGG inhibition of angiogenesis. PGG diminished the phosphorylation of extracellular signal regulated kinase 1/2, Jun NH2-terminal kinase and activated phospho-p38 mitogen-activated protein kinase (MAPK) in a dose-dependent manner in bFGF-treated HUVECs. In addition, p38 inhibitor SB203580 abolished the downregulation of COX-2, VEGF and the antiproliferative activity by PGG. Taken together, our data demonstrate that PGG exerts antitumor activity primarily via inhibition of angiogenesis through COX-2 and MAPK- dependent pathways.


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