alexa Lethariella zahlbruckneri Acetone Extract-Induced Apoptosis of MCF-7 Human Breast Cancer Cells Involves Caspase Cascade and Mitochondria- Mediated Death Signaling | Abstract
ISSN: 2155-9600


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Special Issue Article

Lethariella zahlbruckneri Acetone Extract-Induced Apoptosis of MCF-7 Human Breast Cancer Cells Involves Caspase Cascade and Mitochondria- Mediated Death Signaling

Ju-Hye Lee1, Yeon-Kyong Lee1, Jae-Yong Kim1, Jae-Seoun Hur2, Mi-Kyong Lee1 and Kwon-Il Seo1*

1Department of Food and Nutrition, Sunchon National University, Suncheon 540-742, Republic of Korea

2Korean Lichen Research Institute, Sunchon National University, Suncheon 540-742, Republic of Korea

*Corresponding Author:
Kwon-Il Seo
Department of Food and Nutrition, Sunchon National University
413 Jungangno, Suncheon, Jeonnam, 540-742
Republic of Korea
Tel: +82-61-750-3655
Fax: +82-61-752-3657
E-mail: [email protected]

Received date: May 28, 2012; Accepted date: June 16, 2012; Published date: June 23, 2012

Citation: Lee JH, Lee YK, Kim JY, Jae-Seoun Hur2, Lee MK, et al. (2012) Lethariella Zahlbruckneri Acetone Extract-Induced Apoptosis of MCF-7 Human Breast Cancer Cells Involves Caspase Cascade and Mitochondria-Mediated Death Signaling. J Nutr Food Sci S2:004. doi: 10.4172/2155-9600.S2-004

Copyright: © 2012 Lee JH, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Lethariella zahlbruckneri has been traditionally used in tea and medicines in China. This study aimed to evaluate the anti-cancer properties of L. zahlbruckneri acetone extract (AEL) and to explore its potential mechanisms on MCF- 7 human breast cancer cells. The polyphenol and flavonoid concentrations of were 14.4 mg gallic acid equivalent/g and 6.5 mg quercetin equivalent/g, respectively. AEL inhibited the growth of MCF-7 cells in a dose- and time dependent manner. AEL significantly induced apoptotic cell death, resulting in an increase in the sub-G1 apoptotic cell population, apoptotic DNA fragmentation, and a morphological change. Pretreatment with a caspase inhibitor modestly attenuated the AEL-induced increase in the sub-G1 cell population, implying that caspases play a partial role in AEL-induced apoptosis. Moreover, AEL-induced apoptosis was associated with changes of caspase activities, up-regulation of the apoptotic protein (Bax), and down-regulation of the anti-apoptotic protein (Bcl-2). AEL also induced apoptosis-inducing factor-release from mitochondria, indicating apoptosis stimulation through a caspaseindependent pathway. These results suggest that AEL exerts its anti-cancer effects on MCF-7 human breast cancer cells through mitochondrial caspase-dependent and caspase-independent apoptotic pathways.

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