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Journal of Cancer Prevention

Original Article

Cancer prevention research 2008; 13(3): 169-176

Published online September 30, 2008

© Korean Society of Cancer Prevention

Apoptosis by Quercetin through Induction of Bax and Activation of Caspase in Human Lung Carcinoma Cells

Jun Hyuk Lee1, Su Hyun Hong2, Min Ho Han3, Cheng Yun Jin3, Byung Tae Choi4 and Yung Hyun Choi2,3

Abstract

Quercetin, a plant flavonoid, is widely distributed in fruits and vegetables. This compound has various clinically relevant properties such as anti-oxidant, anti-inflammatory and anti-tumor activity. However, in spite of many reports, the molecular mechanism of quercetin-induced apoptosis in human lung carcinoma cells remains unclear. In this study, we examined the effect of quercetin on the growth and viability using an A549 human lung carcinoma cell line. It was found that quercetin could inhibit the cell growth in a concentration- and dose-dependent manner, which was associated with morphological changes and apoptotic cell death such as rounding up and formation of membrane bleb and spike, apoptotic bodies and increased populations of apoptotic sub-G1 phase. Apoptotic cell death of A549 cells by quercetin was connected with a up-regulation of pro-apoptotic Bax expression and tumor suppressor p53 without alteration of anti-apoptotic Bcl-xL expression. In addition, quercetin treatment induced the proteolytic activation of caspases (caspase-3, -8 and -9) and a concomitant degradation and/or inhibition of poly(ADP-ribose) polymerase (PARP) and Ղ-catenin. Furthermore, caspase inhibitors significantly blocked quercetin-induced growth inhibition demonstrating the important role of caspases in the observed cytotoxic effect. (Cancer Prev Res 13, 169-176, 2008)

Keywords: Quercetin, A549, apoptosis, Bcl-2, caspase

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