Open Access
Article
EGCG inhibits growth, invasion, angiogenesis and metastasis of pancreatic cancer
Sharmila Shankar1,Suthakar Ganapathy1,Sunil R Hingorani1,Rakesh K Srivastava1
1
Department of Biochemistry, University of Texas Health Science Center at Tyler, Tyler, Texas 75703, USA
DOI: 10.2741/2691 Volume 13 Issue 2, pp.440-452
Published: 01 January 2008
(This article belongs to the Special Issue Cancer chemoprevention - 2)
Abstract

We have shown that epigallocatechin-3-gallate (EGCG), a polyphenolic compound from green tea, inhibits growth and induces apoptosis in human pancreatic cancer cells. However, the preclinical potential of EGCG in a suitable mouse model has not been examined. In this study, we examined the molecular mechanisms by which EGCG inhibited growth, invasion, metastasis and angiogenesis of human pancreatic cancer cells in a xenograft model system. EGCG inhibited viability, capillary tube formation and migration of HUVEC, and these effects were further enhanced in the presence of an ERK inhibitor. In vivo, AsPC-1 xenografted tumors treated with EGCG showed significant reduction in volume, proliferation (Ki-67 and PCNA staining), angiogenesis (vWF, VEGF and CD31) and metastasis (MMP-2, MMP-7, MMP-9 and MMP-12) and induction in apoptosis (TUNEL), caspase-3 activity and growth arrest (p21/WAF1). EGCG also inhibited circulating endothelial growth factor receptor 2 (VEGF-R2) positive endothelial cells derived from xenografted mice. Tumor samples from EGCG treated mice showed significantly reduced ERK activity, and enhanced p38 and JNK activities. Overall, our data suggest that EGCG inhibits pancreatic cancer growth, invasion, metastasis and angiogenesis, and thus could be used for the management of pancreatic cancer prevention and treatment.

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Sharmila Shankar, Suthakar Ganapathy, Sunil R Hingorani, Rakesh K Srivastava. EGCG inhibits growth, invasion, angiogenesis and metastasis of pancreatic cancer. Frontiers in Bioscience-Landmark. 2008. 13(2); 440-452.