Apoptosis signal-regulating kinase 1 mediates denbinobin-induced apoptosis in human lung adenocarcinoma cells

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TMUIR > College of Medicine > Department of Medicine > Department of Microbiology and Immunology > Periodical Article > Item 987654321/1053

Please use this identifier to cite or link to this item: http://libir.tmu.edu.tw/handle/987654321/1053

Title:	Apoptosis signal-regulating kinase 1 mediates denbinobin-induced apoptosis in human lung adenocarcinoma cells
Authors:	陳玫潔 Kuo CT;Chen BC;Hsu MJ;Chen CC;Chen MC;Teng CM;Pan SL;Bien MY;Shih SH;Lin CH
Contributors:	醫學系微生物與免疫學科
Date:	2008
Issue Date:	2009-08-14 10:37:42 (UTC+8)
Abstract:	In the present study, we explore the role of apoptosis signal-regulating kinase 1 (ASK1) in denbinobin-induced apoptosis in human lung adenocarcinoma (A549) cells. Denbinobin-induced cell apoptosis was attenuated by an ASK1 dominant-negative mutant (ASK1DN), two antioxidants (N-acetyl-L-cysteine (NAC) and glutathione (GSH)), a c-Jun N-terminal kinase (JNK) inhibitor (SP600125), and an activator protein-1 (AP-1) inhibitor (curcumin). Treatment of A549 cells with denbinobin caused increases in ASK1 activity and reactive oxygen species (ROS) production, and these effects were inhibited by NAC and GSH. Stimulation of A549 cells with denbinobin caused JNK activation; this effect was markedly inhibited by NAC, GSH, and ASK1DN. Denbinobin induced c-Jun phosphorylation, the formation of an AP-1-specific DNA-protein complex, and Bim expression. Bim knockdown using a bim short interfering RNA strategy also reduced denbinobin-induced A549 cell apoptosis. The denbinobin-mediated increases in c-Jun phosphorylation and Bim expression were inhibited by NAC, GSH, SP600125, ASK1DN, JNK1DN, and JNK2DN. These results suggest that denbinobin might activate ASK1 through ROS production to cause JNK/AP-1 activation, which in turn induces Bim expression, and ultimately results in A549 cell apoptosis.
Relation:	Journal of Biomedical Science.(submit)
Data Type:	article
Appears in Collections:	[Department of Microbiology and Immunology] Periodical Article

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