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BA6 Induces Apoptosis via Stimulation of Reactive Oxygen Species and Inhibition of Oxidative Phosphorylation in Human Lung Cancer Cells
Joint Authors
Tsui, Kuan-Hao
Kuo, Hsiao-Mei
Wen, Zhi-Hong
Chong, Inn-Wen
Sung, Ping-Jyun
Cheng, Meng-Hsuan
Huang, Hung-Ling
Lin, Yen-You
Chen, Pei-Chin
Cheng, Shu-Yu
Tai, Ming-Hong
Chen, Nan-Fu
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-21, 21 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-05-07
Country of Publication
Egypt
No. of Pages
21
Main Subjects
Abstract EN
Lung cancer is the leading cause of cancer deaths in the world, with a five-year survival rate of less than 30%.
Clinically effective chemotherapeutic treatments at the initial stage may eventually face the dilemma of no drug being effective due to drug resistance; therefore, finding new effective drugs for lung cancer treatment is a necessary and important issue.
Compounds capable of further increasing the oxidative stress of cancer cells are considered to have anticancer potential because they possessed the ability to induce apoptosis.
This study mainly investigated the effects of BA6 (heteronemin), the marine sponge sesterterpene, on lung cancer cell apoptosis, via modulation of mitochondrial reactive oxygen species (mtROS) and oxidative phosphorylation (OXPHOS).
BA6 has cellular cytotoxic activities against a variety of cancer cell lines, but it has no effect on nontumor cells.
The BA6-treated lung cancer cells show a significant increase in both cellular ROS and mtROS, which in turn caused the loss of mitochondrial membrane potential (MMP).
The increase of oxidative stress in lung cancer cells treated with BA6 was accompanied by a decrease in the expression of antioxidant enzymes Cu/Zn SOD, MnSOD, and catalase.
In addition, OXPHOS performed in the mitochondria and glycolysis in the cytoplasm were inhibited, which subsequently reduced downstream ATP production.
Pretreatment with mitochondria-targeted antioxidant MitoTEMPO reduced BA6-induced apoptosis through the mitochondria-dependent apoptotic pathway, which was accompanied by increased cell viability, decreased mtROS, enhanced MMP, and suppressed expression of cleaved caspase-3 and caspase-9 proteins.
In conclusion, the results of this study clarify the mechanism of BA6-induced apoptosis in lung cancer cells via the mitochondrial apoptotic pathway, suggesting that it is a potentially innovative alternative to the treatment of human lung cancer.
American Psychological Association (APA)
Cheng, Meng-Hsuan& Huang, Hung-Ling& Lin, Yen-You& Tsui, Kuan-Hao& Chen, Pei-Chin& Cheng, Shu-Yu…[et al.]. 2019. BA6 Induces Apoptosis via Stimulation of Reactive Oxygen Species and Inhibition of Oxidative Phosphorylation in Human Lung Cancer Cells. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-21.
https://search.emarefa.net/detail/BIM-1204554
Modern Language Association (MLA)
Cheng, Meng-Hsuan…[et al.]. BA6 Induces Apoptosis via Stimulation of Reactive Oxygen Species and Inhibition of Oxidative Phosphorylation in Human Lung Cancer Cells. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-21.
https://search.emarefa.net/detail/BIM-1204554
American Medical Association (AMA)
Cheng, Meng-Hsuan& Huang, Hung-Ling& Lin, Yen-You& Tsui, Kuan-Hao& Chen, Pei-Chin& Cheng, Shu-Yu…[et al.]. BA6 Induces Apoptosis via Stimulation of Reactive Oxygen Species and Inhibition of Oxidative Phosphorylation in Human Lung Cancer Cells. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-21.
https://search.emarefa.net/detail/BIM-1204554
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1204554