Magnolol induces apoptosis via activation of both mitochondrial and death receptor pathways in A375-S2 cells.

Qingjun You, Mingqiu Li, Guoqing Jiao

Journal: Archives of pharmacal research 2010;32(12):1789-94

PMID: 20162409

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Abstract

Magnolol inhibited proliferation of human malignant melanoma A375-S2 cells. The drug induced oligonucleosomal fragmentation of DNA in A375-S2 cells and increased caspase-3, 8, 9 activities followed by the degradation of caspase-3 substrates, inhibitor of caspase dependent DNase (ICAD) and poly-(ADP-ribose) polymerase (PARP). Pan-caspase inhibitor (z-VADfmk), caspase-3 inhibitor (z-DEVD-fmk), capase-8 inhibitor (z-IETD-fmk), caspase-9 inhibitor (z-LEHD-fmk) and caspase-10 inhibitor (z-AEVD-fmk) inhibited magnolol-induced A375-S2 cell apoptosis. The level of anti-apoptotic mitochondrial protein Bcl-2 was up-regulated while the level of pro-apoptotic protein Bax was down-regulated. Taken together, our results indicate that magnolol induces apoptosis by activation of both mitochondrial and death receptor pathways in A375-S2 cells.

Address: Department of Cardiothoracic Surgery, Wuxi The Forth Hospital, Wuxi City Huihe Road 200, 214062, Wuxi, China.

DOI: 10.1007/s12272-009-2218-6

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MeSH Terms: Antineoplastic Agents, Phytogenic, Apoptosis, Biphenyl Compounds, Bisbenzimidazole, Blotting, Western, Caspase 3, Caspase 8, Caspase 9, Cell Line, Tumor, Cell Nucleus, Cell Survival, Coloring Agents, DNA Fragmentation, DNA, Neoplasm, Humans, Lignans, Melanoma, Experimental, Mitochondria, Proto-Oncogene Proteins c-bcl-2, Receptors, Death Domain, Signal Transduction, bcl-2-Associated X Protein, fas Receptor