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Bid integrates intrinsic and extrinsic signaling in apoptosis induced by alpha-tocopheryl succinate in human gastric carcinoma cells
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SYSNO ASEP 0340714 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Bid integrates intrinsic and extrinsic signaling in apoptosis induced by alpha-tocopheryl succinate in human gastric carcinoma cells Author(s) Zhao, Y. (CN)
Li, R. (CN)
Xia, W. (CN)
Neužil, Jiří (BTO-N) RID
Lu, Y. (CN)
Zhang, H. (CN)
Zhao, X. (CN)
Zhang, X. (CN)
Sun, C. (CN)
Wu, K. (CN)Source Title Cancer letters. - : Elsevier - ISSN 0304-3835
Roč. 288, č. 1 (2010), s. 42-49Number of pages 8 s. Language eng - English Country IE - Ireland Keywords Alpha-tocopheryl succinate ; signaling ; apoptosis Subject RIV EB - Genetics ; Molecular Biology R&D Projects GA204/08/0811 GA ČR - Czech Science Foundation (CSF) CEZ AV0Z50520701 - BTO-N (2007-2013) UT WOS 000274991700006 DOI 10.1016/j.canlet.2009.06.021 Annotation The underlying mechanisms of alpha-tocopheryl succinate (alpha-TOS)-mediated apoptosis are not understood in detail, although the redox-silent vitamin E analog is a potent apoptogen and anti-cancer agent. The objective of the present study was to investigate whether apoptosis triggered by alpha-TOS in gastric carcinomas cells involves both mitochondria- and death receptor-dependent pathways. alpha-TOS induced apoptosis and mitochondrial permeability transition in a concentration- and time-dependent manner. As a consequence, cytochrome c and the apoptosis-inducing factor were released and caspases were activated. Bax was translocated from the cytosol to mitochondria and Bid was cleaved into its truncated form, tBid. Knocking down Bid by RNAi and Fas antisense oligodeoxynucleotides resulted in a decreased release and cleavage. The results imply that Bid may serve as a critical integrating factor of the death receptor and mitochondrial pathway in alpha-TOS-mediated apoptosis. Workplace Institute of Biotechnology Contact Monika Kopřivová, Monika.Koprivova@ibt.cas.cz, Tel.: 325 873 700 Year of Publishing 2010
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