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Evidence-Based Complementary and Alternative Medicine
Volume 2013 (2013), Article ID 548929, 11 pages
Research Article

Destruxin B Isolated from Entomopathogenic Fungus Metarhizium anisopliae Induces Apoptosis via a Bcl-2 Family-Dependent Mitochondrial Pathway in Human Nonsmall Cell Lung Cancer Cells

1Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan
2Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan
3Department of Health and Nutrition, Chia Nan University of Pharmacy & Science, Tainan, Taiwan
4Department of Applied Chemistry, Chaoyang University of Technology, Taichung, Taiwan
5Department of Applied Chemistry, National Chi Nan University, Puli, Nantou, Taiwan
6Department of Education and Research, Taichung Veterans General Hospital, Taichung, Taiwan

Received 20 March 2013; Accepted 20 August 2013

Academic Editor: Mei Tian

Copyright © 2013 Chun-Chi Wu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Destruxin B, isolated from entomopathogenic fungus Metarhizium anisopliae, is one of the cyclodepsipeptides with insecticidal and anticancer activities. In this study, destruxin B was extracted and purified by ion-exchange chromatography, silica gel chromatography, and semipreparative high-performance liquid chromatography. The potential anticancer effects and molecular mechanisms of destruxin B in human nonsmall cell lung cancer cell lines were characterized. Our results showed that destruxin B induced apoptotic cell death in A549 cells. This event was accompanied by the activation of caspase-2, -3, and -9. Moreover, destruxin B increased the expression level of proapoptotic molecule, PUMA, while decreased antiapoptotic molecule Mcl-1. Additionally, the translocation of Bax from cytosol to mitochondrial membrane was observed upon destruxin B treatment. Knockdown of Bax by shRNA effectively attenuated destruxin-B-triggered apoptosis in A549 cells. Interestingly, similar toxic effects and underlying mechanisms including caspase activation, upregulation of PUMA, and downregulation of Mcl-1 were also observed in a p53-null lung cancer H1299 cell line upon destruxin B treatment. Taken together, our findings suggest that destruxin-B-induced apoptosis in human nonsmall cell lung cancer cells is via a Bcl-2 family-dependent mitochondrial pathway.