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Mar. Drugs 2013, 11(2), 418-430; doi:10.3390/md11020418
Article

Cytotoxic Effect of Clerosterol Isolated from Codium fragile on A2058 Human Melanoma Cells

1
, 1
, 2
, 2
, 3
 and 1,*
1 School of Medicine, Jeju National University, Jeju 690-756, Korea 2 Department of Marine Life Sciences, Jeju National University, Jeju 690-756, Korea 3 Cancer Research Institute, Seoul National University College of Medicine, Seoul 110-799, Korea
* Author to whom correspondence should be addressed.
Received: 18 December 2012 / Revised: 21 January 2013 / Accepted: 31 January 2013 / Published: 6 February 2013
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Abstract

The cytotoxic effects and mechanism of action of clerosterol, isolated from the marine alga Codium fragile, were investigated in A2058 human melanoma cells. Clerosterol inhibited the growth of A2058 cells with an IC50 of 150 µM and induced apoptotic cell death, as evidenced by DNA fragmentation, an increase in the number of sub-G1 hypodiploid cells and the presence of apoptotic bodies. Clerosterol treatment caused the loss of mitochondrial membrane potential. Alterations in the expression of apoptosis-associated proteins in response to clerosterol treatment included upregulation of Bax, downregulation of Bcl-2 and activation of caspases 3 and 9. The pan-caspase inhibitor treatment attenuated the expression of the active form of caspases and cell death induced by clerosterol. The present results show that clerosterol exerts its cytotoxic effect in A2058 human melanoma cells by caspases-dependent apoptosis.
Keywords: clerosterol; melanoma cell; apoptosis; mitochondrial membrane potential clerosterol; melanoma cell; apoptosis; mitochondrial membrane potential
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.

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Kim, A.D.; Lee, Y.; Kang, S.-H.; Kim, G.Y.; Kim, H.S.; Hyun, J.W. Cytotoxic Effect of Clerosterol Isolated from Codium fragile on A2058 Human Melanoma Cells. Mar. Drugs 2013, 11, 418-430.

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