Premium
Oral Administration of EGCG, an Antioxidant Found in Green Tea, Inhibits Tumor Angiogenesis and Growth of Breast Cancer in Female Mice
Author(s) -
Gu JianWei,
Young Emily,
Covington Jordan,
Johnson James Wes,
Tan Wei
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1164.3
Subject(s) - angiogenesis , cd31 , breast cancer , vascular endothelial growth factor , medicine , immunohistochemistry , cancer , neovascularization , oxidative stress , endocrinology , antioxidant , malignancy , cancer research , chemistry , vegf receptors , biochemistry
Oxidative stress has been implicated in promoting growth and malignancy of cancers including breast cancer. We evaluated whether oral administration of epigallocatechin‐3‐gallate (EGCG), an antioxidant found in green tea, inhibits vascular endothelial growth factor (VEGF) expression, tumor angiogenesis, and growth of breast cancer in female mice. 7‐wk‐old female mice (C57BL) were given EGCG 25mg/50ml in drinking water for 5 wks, which was around 50–100 mg/kg/day. The control mice received regular drinking water. In the 2nd wk, ~1×10^5 E0771 (mouse breast cancer) cells were injected in 4th mammary gland of the mice. Tumor size was monitored by measuring tumor cross section area (TCSA). In the end, the tumors were isolated for measuring tumor weight, intratumoral microvessel (IM) density using CD31 immunohistochemistry staining, and VEGF protein levels using ELISA. Oral EGCG treatment caused the significant decreases in TCSA (66%), in tumor weight (68%), in IM density (155±6 vs. 111±20 IM#/mm^2), and in VEGF protein levels (59.0±3.7 vs. 45.7±1.4 pg/mg) of breast tumors, compared to the control, respectively (N = 8; P<0.01). VEGF plasma levels were lower in EGCG mice than control mice (40.8±3.5 vs. 26.5±3.8 pg/ml; P<0.01). The results suggest that antioxidant treatment with EGCG significantly inhibits breast cancer progression via reducing VEGF expression and tumor angiogenesis. (NIH/AA013821 & NIH/HL 51971)