EGCG inhibits growth, invasion, angiogenesis, metastasis of pancreatic cancer

EGCG inhibits growth, invasion, angiogenesis, metastasis of pancreatic cancer

* w w w .ncbi.nlm.nih.gov/pubmed/17981559?ordinalpos=77&itool=EntrezSystem
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Front Biosci. 2008 Jan 1;13:440-52

EGCG inhibits growth, invasion, angiogenesis and metastasis of pancreatic
cancer.

Shankar S, Ganapathy S, Hingorani SR, Srivastava RK.
Department of Biochemistry, University of Texas Health Science Center at
Tyler, Tyler, Texas 75703, USA.

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.