Journal
NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL
Volume 66, Issue 4, Pages 728-735Publisher
ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
DOI: 10.1080/01635581.2013.783601
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- Ministry of Education, Science, Sports and Culture of Japan [19590757]
- Grants-in-Aid for Scientific Research [19590757] Funding Source: KAKEN
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It is agreed that many of the antitumor effects of (-)-epigallocatechin gallate (EGCG) are mediated by various other effects. We report a new finding, namely, the antiproliferation potential and mechanism of methylated-(3)-epigallocatechin gallate analog (MethylEGCG) having a stronger anti-oxidation effect than EGCG. MethylEGCG inhibited activity of vascular endothelial growth factor (VEGF)-depended VEGF receptor 2 and p42/44 MAPK, cell proliferation, and tube formation in human umbilical vascular endothelial cells (HUVECs) at 1 M. Even low- dose (1.1mg/kg i.p. 8.3mg/kg p.o.) administration suppressed tumor growth in xenografted Huh7 hepatoma mice by 50%. CD31 positive cells, visualized in blood vessels, were reduced in tumors by 18%, suggesting high antitumor activity via inhibition of angiogenesis. This study indicated that the modification of the 3 position methylation of EGCG (MethylEGCG) could reduce cell growth effects at a low concentration in vivo.
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