title: Inhibition of fibroblast growth factors by green tea.
abstract: Investigators have shown that green tea may decrease the risk of cancer. It is widely accepted that the main active component of green tea is EGCG (epigallocatechin-3-gallate). In our previous study, we examined the effect of green tea on breast cancer growth and endothelial cells both in in vitro assays and in animal models. Our data show that both mixed green tea extract (GTE) as well as its individual catechin components are effective in inhibiting breast cancer and endothelial cell proliferation in vitro, and that GTE suppresses breast cancer xenograft size and decreases the tumor blood vessel density in vivo. In the present study, we further demonstrate that 40 microg/ml GTE or EGCG can decrease the levels of the angiogenic factor bFGF (basic fibroblast growth factor) levels in the cells. This phenomenon is observed in both human umbilical vein endothelial cells (HUVECs) and in human breast cancer cells MDA-MB231. This effect is dose dependent. Furthermore, GTE and EGCG decrease the transcript levels of bFGF and aFGF (acidic fibroblast growth factor) in HUVECs and MDA-MB231 cells. Our findings suggest that the inhibition of the angiogenic fibroblast growth factors could account for one of the mechanisms of green tea's actions. Since cancer is angiogenesis dependent, this may partially explain the antineoplastic effects associated with green tea consumption.
authors.affiliation: Department of Surgery, Division of Oncology, University of California-Los Angeles, Los Angeles, CA 90095, USA.
authors.forename: Maryam R
authors.initials: MR
authors.lastname: Sartippour
authors.forename: David
authors.initials: D
authors.lastname: Heber
authors.forename: Liping
authors.initials: L
authors.lastname: Zhang
authors.forename: Perrin
authors.initials: P
authors.lastname: Beatty
authors.forename: David
authors.initials: D
authors.lastname: Elashoff
authors.forename: Robert
authors.initials: R
authors.lastname: Elashoff
authors.forename: Vay Liang
authors.initials: VL
authors.lastname: Go
authors.forename: Mai N
authors.initials: MN
authors.lastname: Brooks
mesh_terms: D020533:Angiogenesis Inhibitors / Q000494:pharmacology*; D000970:Antineoplastic Agents / Q000494:pharmacology*; D001943:Breast Neoplasms / Q000098:blood supply / Q000188:drug therapy / Q000378:metabolism; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology*; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism; D016220:Fibroblast Growth Factor 1 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D016222:Fibroblast Growth Factor 2 / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D006801:Humans; D009389:Neovascularization, Pathologic / Q000188:drug therapy / Q000378:metabolism; D010936:Plant Extracts / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D013662:Tea / Q000737:chemistry*
chemical_list: D020533:Angiogenesis Inhibitors; D000970:Antineoplastic Agents; D010936:Plant Extracts; D012333:RNA, Messenger; D013662:Tea; D016222:Fibroblast Growth Factor 2; D016220:Fibroblast Growth Factor 1; D002392:Catechin; C045651:epigallocatechin gallate