방사선의학 웹진

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Abstract

Benzylideneacetophenone derivative (1E)-1-(4-hydroxy-3-methoxyphenyl) hept-1-en-3-one (JC3) elicited cytotoxic effects on MDA-MB 231 human breast cancer cells-radiation resistant cells (MDA-MB 231-RR), in a dose-dependent manner, with an IC50 value of 6 µM JC3. JC3-mediated apoptosis was confirmed by increase in sub-G1 cell population. JC3 disrupted the mitochondrial membrane potential, and reduced expression of anti-apoptotic B cell lymphoma-2 protein, whereas it increased expression of pro-apoptotic Bcl-2-associated X protein, leading to the cleavage of caspase-9, caspase-3 and poly (ADP-ribose) polymerase. In addition, JC3 activated mitogen-activated protein kinases, and specific inhibitors of these kinases abrogated the JC3-induced increase in apoptotic bodies. JC3 increased the level of intracellular reactive oxygen species and enhanced oxidative macromolecular damage via lipid peroxidation, protein carbonylation, and DNA strand breakage. Considering these findings, JC3 is an effective therapy against radiation-resistant human breast cancer cells. 

Author information

Park JE1, Piao MJ1, Kang KA1, Shilnikova K1, Hyun YJ1, Oh SK2, Jeong YJ3, Chae S4, Hyun JW1.​

1School of Medicine and Institute for Nuclear Science and Technology, Jeju National University, Jeju 63243, Republic of Korea.2Department of Neuroscience, College of Medicine, Ewha Womans University, Seoul 03760, Republic of Korea.3Department of Bio and Nanochemistry, Kookmin University, Seoul 02707, Republic of Korea.4Aging Research Center, Korea Institute of Oriental Medicine, Daejeon 34054, Republic of Korea.