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Carcinogenesis Advance Access published online on February 10, 2005
Carcinogenesis, doi:10.1093/carcin/bgi040
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oupjournals.org
Received July 26, 2004
Revised January 11, 2005
Accepted January 28, 2005

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Epigallocatechin-3-gallate induces mitochondrial membrane depolarization and caspase-dependent apoptosis in pancreatic cancer cells

Suparna Qanungo 1, Madhusudan Das 1, Subrata Haldar 1, and Aruna Basu 1*

1 Dept of Research, Pharmacology, Case Comprehensive Cancer Center, MetroHealth Medical Center, Case Western Reserve University, Cleveland, OH 44109, USA

* To whom correspondence should be addressed.
Aruna Basu, E-mail: Abasu{at}metrohealth.org


  Abstract

Polyphenols such as epigallocatechin-3-gallate (EGCG) from green tea extract can exert growth-suppressive effect on human pancreatic cancer cells in vitro. In pursuit to our investigations to dissect the molecular mechanism of EGCG action on pancreatic cancer, we observed that the antiproliferative action of EGCG on pancreatic carcinoma is mediated through programmed cell death or apoptosis as evident from nuclear condensation, caspase-3 activation and PARP cleavage. EGCG-induced apoptosis of pancreatic cancer cells is accompanied by growth arrest at earlier phase of the cell cycle. In addition, EGCG invokes Bax oligomerization and depolarization of mitochondrial membranes to facilitate cytochrome c release into cytosol. EGCG induced down regulation of IAP family member XIAP might be helpful to facilitate cytochrome c mediated downstream caspase activation. To the other end, EGCG elicited production of intracellular reactive oxygen species (ROS) as well as JNK activation in pancreatic carcinoma cells. Interestingly, inhibitor of JNK signaling pathway as well as antioxidant N- acetyl-L-cysteine (NAC) blocked EGCG-induced apoptosis. To summarize, our studies suggest that EGCG induces stress signals by damaging mitochondria and ROS-mediated JNK activation in MIA PaCa-2 pancreatic carcinoma cells.

Keywords: epigallocatechin-3-gallate; apoptosis; chemopreventive agent; pancreatic cancer.
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