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Carcinogenesis Advance Access originally published online on February 10, 2005
Carcinogenesis 2005 26(5):958-967; doi:10.1093/carcin/bgi040
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Carcinogenesis vol.26 no.5 © Oxford University Press 2005; all rights reserved.

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

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

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

* To whom correspondence should be addressed at: R455, Rammelkamp Building, MetroHealth Medical Center, 2500 MetroHealth Drive, Cleveland, OH 44109, USA. Tel: +216 778 2429; Fax: +216 778 4321; Email: Abasu{at}metrohealth.org

Polyphenols such as epigallocatechin-3-gallate (EGCG) from green tea extract can exert a growth-suppressive effect on human pancreatic cancer cells in vitro. In pursuit of 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 poly-ADP ribose polymerase (PARP) cleavage. EGCG-induced apoptosis of pancreatic cancer cells is accompanied by growth arrest at an 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 downregulation of IAP family member X chromosome linked inhibitor of apoptosis protein (XIAP) might be helpful to facilitate cytochrome c mediated downstream caspase activation. On the other end, EGCG elicited the production of intracellular reactive oxygen species (ROS), as well as the c-Jun N-terminal kinase (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.


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