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Mar. Drugs 2017, 15(7), 210; doi:10.3390/md15070210

24-Methyl-Cholesta-5,24(28)-Diene-3β,19-diol-7β-Monoacetate Inhibits Human Small Cell Lung Cancer Growth In Vitro and In Vivo via Apoptosis Induction

1
Department of Medical Sciences, Institute of Bioinformatics and Structural Biology, National Tsing Hua University, Hsinchu 300, Taiwan
2
Taiwan Coral Research Center, National Museum of Marine Biology & Aquarium, Pingtung 944, Taiwan
3
Department of Life Sciences, Institute of Biomedical Science, National Chung Hsing University, Taichung 402, Taiwan
4
Department of Internal Medicine, Changhua Christian Hospital, Changhua Division of Chest Medicine, Changhua 500, Taiwan
*
Authors to whom correspondence should be addressed.
Received: 19 April 2017 / Revised: 13 June 2017 / Accepted: 26 June 2017 / Published: 1 July 2017
(This article belongs to the Special Issue Natural Products from Coral Reef Organisms)
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Abstract

24-methyl-cholesta-5,24(28)-diene-3β,19-diol-7β-monoacetate (MeCDDA) is a natural steroid compound isolated from a wild-type soft coral (Nephthea erecta). The present study aimed to investigate the anti-small cell lung cancer (SCLC) effects of MeCDDA in vitro and in vivo, as well as to elucidate its underlying mechanism. Our results indicated that H1688 and H146 cells show relevant sensitivity to MeCDDA, and the exposure to MeCDDA in SCLC cells caused dose-dependent growth inhibitory responses. In addition, MeCDDA treatment promoted cell apoptosis and increased the activities of caspases in H1688 cells, reducing the mitochondrial membrane potential and stimulating the release of cytochrome c into the cytosol. Along with the increase in Bax expression and reduction in Bcl-2, the MeCDDA treatment also significantly decreased Akt and mTOR phosphorylation. Finally, MeCDDA treatment in the mouse xenograft model of H1688 cells exhibited significant inhibition of tumor growth, corroborating MeCDDA as a potential pre-clinical candidate for the treatment of SCLC. Overall, our results demonstrate that the cytotoxic effects of MeCDDA towards H1688 and H146 cells, possibly through the activation of the mitochondrial apoptotic pathway and inhibition of the PI3K/Akt/mTOR pathway, merit further studies for its possible clinical application in chemotherapy. View Full-Text
Keywords: 24-methyl-cholesta-5,24(28)-diene-3β,19-diol-7β-monoacetate; MeCDDA; Nephthea erecta; small cell lung cancer; apoptosis 24-methyl-cholesta-5,24(28)-diene-3β,19-diol-7β-monoacetate; MeCDDA; Nephthea erecta; small cell lung cancer; apoptosis
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Chung, T.-W.; Su, J.-H.; Lin, C.-C.; Li, Y.-R.; Chao, Y.-H.; Lin, S.-H.; Chan, H.-L. 24-Methyl-Cholesta-5,24(28)-Diene-3β,19-diol-7β-Monoacetate Inhibits Human Small Cell Lung Cancer Growth In Vitro and In Vivo via Apoptosis Induction. Mar. Drugs 2017, 15, 210.

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