Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/74661
Title: A prodrug of green tea polyphenol (–)-epigallocatechin-3-gallate (Pro-eGCG) serves as a novel angiogenesis inhibitor in endometrial cancer
Authors: Wang, J
Man, GCW
Chan, TH 
Kwong, J
Wang, CC
Keywords: Angiogenesis
Endometrial cancer
Hypoxia inducible factor 1 alpha
Pro-EGCG
Tumor-associated macrophages
Issue Date: 2018
Publisher: Elsevier
Source: Cancer letters, 2018, v. 412, p. 10-20 How to cite?
Journal: Cancer letters 
Abstract: Anti-angiogenesis effect of a prodrug of green tea polyphenol (–)-epigallocatechin-3-gallate (Pro-EGCG) in malignant tumors is not well studied. Here, we investigated how the treatment with Pro-EGCG inhibited tumor angiogenesis in endometrial cancer. Tumor xenografts of human endometrial cancer were established and subjected to microarray analysis after Pro-EGCG treatment. First, we showed Pro-EGCG inhibited tumor angiogenesis in xenograft models through down-regulation of vascular endothelial growth factor A (VEGFA) and hypoxia inducible factor 1 alpha (HIF1α) in tumor cells and chemokine (C-X-C motif) ligand 12 (CXCL12) in host stroma by immunohistochemical staining. Next, we investigated how HIF1α/VEGFA was down-regulated and how the reduction of CXCL12 inhibited tumor angiogenesis. We found that VEGFA secretion from endometrial cancer cells was decreased by Pro-EGCG treatment through inhibiting PI3K/AKT/mTOR/HIF1α pathway. Furthermore, the down-regulation of CXCL12 in stromal cells by Pro-EGCG treatment restricted migration and differentiation of macrophages thereby inhibited infiltration of VEGFA-expressing tumor-associated macrophages (TAMs). Taken together, we demonstrated that treatment with Pro-EGCG not only decreases cancer cell-secreted VEGFA but also inhibits TAM-secreted VEGFA in endometrial cancer. These findings demonstrate that Pro-EGCG is a novel angiogenesis inhibitor for endometrial cancer.
URI: http://hdl.handle.net/10397/74661
ISSN: 0304-3835
EISSN: 0304-3835
DOI: 10.1016/j.canlet.2017.09.054
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