Journal
LUNG CANCER
Volume 65, Issue 2, Pages 150-160Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.lungcan.2008.11.005
Keywords
Antimycin A; ROS; Apoptosis; Calu-6; Caspase; Mitochondria
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Funding
- Chonbuk National University Medical School Alumni
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Antimycin A (AMA) inhibits mitochondrial electron transport between cytochrome b and c. We evaluated the effects of AMA on the growth of human lung cancer cell line, Calu-6. AMA inhibited the growth of Calu-6 cells. AMA induced a G1 phase arrest of the cell cycle in these cells at 72 h. AMA increased a cyclin-dependent kinase inhibitor (CDKI), p27 and decreased CDK2, CDK4, and CDK6, as well as cyclin D1 and cyclin E in Calu-6 cells. AMA also induced apoptosis in Calu-6 cells. The apoptotic process in AMA-treated Calu-6 cells was accompanied by the up-regulation of Bax, the loss of mitochondrial membrane potential (Delta Psi(m)), and the activation of caspase-3 and -8. All of the tested caspase inhibitors, especially pan-caspase inhibitor (Z-VAD), markedly rescued Calu-6 cells from AMA-induced Calu-6 cell death. Inhibitors of pan-caspase and caspase-8 also prevented the loss of mitochondrial membrane potential (Delta Psi(m)). AMA decreased the intracellular ROS levels but increased the O-2(center dot-) levels in Calu-6 cells. In conclusion, AMA as a mitochondrial electron transport inhibitor decreased the growth of lung cancer Calu-6 cell via inducing a G1 arrest of the cell cycle and apoptosis. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
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