Induction of Apoptosis by Costunolide in Bladder Cancer Cells is Mediated through ROS Generation and Mitochondrial Dysfunction

Despite the availability of several therapeutic options, a safer and more effective modality is urgently needed for treatment of bladder cancer. Costunolide, a member of sesquiterpene lactone family, possesses potent anticancer properties. In this study, for the first time we investigated the effect...
Ausführliche Beschreibung

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Autor*in:	Ichiro Tsuji [verfasserIn] Jiang Li [verfasserIn] Bing Zhao [verfasserIn] Mahadev Malhi [verfasserIn] Rui Bao [verfasserIn] Azhar Rasul [verfasserIn] Xiaomeng Li [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2013

Schlagwörter:	bladder cancer T24 cells costunolide apoptosis reactive oxygen species

Übergeordnetes Werk:	In: Molecules - MDPI AG, 2003, 18(2013), 2, Seite 1418-1433
Übergeordnetes Werk:	volume:18 ; year:2013 ; number:2 ; pages:1418-1433

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/molecules18021418

Katalog-ID:	DOAJ01147694X

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650		4	\|a bladder cancer
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language	English
source	In Molecules 18(2013), 2, Seite 1418-1433 volume:18 year:2013 number:2 pages:1418-1433
sourceStr	In Molecules 18(2013), 2, Seite 1418-1433 volume:18 year:2013 number:2 pages:1418-1433
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	bladder cancer T24 cells costunolide apoptosis reactive oxygen species Organic chemistry
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container_title	Molecules
authorswithroles_txt_mv	Ichiro Tsuji @@aut@@ Jiang Li @@aut@@ Bing Zhao @@aut@@ Mahadev Malhi @@aut@@ Rui Bao @@aut@@ Azhar Rasul @@aut@@ Xiaomeng Li @@aut@@
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callnumber-first	Q - Science
author	Ichiro Tsuji
spellingShingle	Ichiro Tsuji misc QD241-441 misc bladder cancer misc T24 cells misc costunolide misc apoptosis misc reactive oxygen species misc Organic chemistry Induction of Apoptosis by Costunolide in Bladder Cancer Cells is Mediated through ROS Generation and Mitochondrial Dysfunction
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topic_title	QD241-441 Induction of Apoptosis by Costunolide in Bladder Cancer Cells is Mediated through ROS Generation and Mitochondrial Dysfunction bladder cancer T24 cells costunolide apoptosis reactive oxygen species
topic	misc QD241-441 misc bladder cancer misc T24 cells misc costunolide misc apoptosis misc reactive oxygen species misc Organic chemistry
topic_unstemmed	misc QD241-441 misc bladder cancer misc T24 cells misc costunolide misc apoptosis misc reactive oxygen species misc Organic chemistry
topic_browse	misc QD241-441 misc bladder cancer misc T24 cells misc costunolide misc apoptosis misc reactive oxygen species misc Organic chemistry
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title	Induction of Apoptosis by Costunolide in Bladder Cancer Cells is Mediated through ROS Generation and Mitochondrial Dysfunction
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title_full	Induction of Apoptosis by Costunolide in Bladder Cancer Cells is Mediated through ROS Generation and Mitochondrial Dysfunction
author_sort	Ichiro Tsuji
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title_sort	induction of apoptosis by costunolide in bladder cancer cells is mediated through ros generation and mitochondrial dysfunction
callnumber	QD241-441
title_auth	Induction of Apoptosis by Costunolide in Bladder Cancer Cells is Mediated through ROS Generation and Mitochondrial Dysfunction
abstract	Despite the availability of several therapeutic options, a safer and more effective modality is urgently needed for treatment of bladder cancer. Costunolide, a member of sesquiterpene lactone family, possesses potent anticancer properties. In this study, for the first time we investigated the effects of costunolide on the cell viability and apoptosis in human bladder cancer T24 cells. Treatment of T24 cells with costunolide resulted in a dose-dependent inhibition of cell viability and induction of apoptosis which was associated with the generation of ROS and disruption of mitochondrial membrane potential (Δψm). These effects were significantly blocked when the cells were pretreated with N-acetyl- cysteine (NAC), a specific ROS inhibitor. Exposure of T24 cells to costunolide was also associated with increased expression of Bax, down-regulation of Bcl-2, survivin and significant activation of caspase-3, and its downstream target PARP. These findings provide the rationale for further in vivo and clinical investigation of costunolide against human bladder cancer.
abstractGer	Despite the availability of several therapeutic options, a safer and more effective modality is urgently needed for treatment of bladder cancer. Costunolide, a member of sesquiterpene lactone family, possesses potent anticancer properties. In this study, for the first time we investigated the effects of costunolide on the cell viability and apoptosis in human bladder cancer T24 cells. Treatment of T24 cells with costunolide resulted in a dose-dependent inhibition of cell viability and induction of apoptosis which was associated with the generation of ROS and disruption of mitochondrial membrane potential (Δψm). These effects were significantly blocked when the cells were pretreated with N-acetyl- cysteine (NAC), a specific ROS inhibitor. Exposure of T24 cells to costunolide was also associated with increased expression of Bax, down-regulation of Bcl-2, survivin and significant activation of caspase-3, and its downstream target PARP. These findings provide the rationale for further in vivo and clinical investigation of costunolide against human bladder cancer.
abstract_unstemmed	Despite the availability of several therapeutic options, a safer and more effective modality is urgently needed for treatment of bladder cancer. Costunolide, a member of sesquiterpene lactone family, possesses potent anticancer properties. In this study, for the first time we investigated the effects of costunolide on the cell viability and apoptosis in human bladder cancer T24 cells. Treatment of T24 cells with costunolide resulted in a dose-dependent inhibition of cell viability and induction of apoptosis which was associated with the generation of ROS and disruption of mitochondrial membrane potential (Δψm). These effects were significantly blocked when the cells were pretreated with N-acetyl- cysteine (NAC), a specific ROS inhibitor. Exposure of T24 cells to costunolide was also associated with increased expression of Bax, down-regulation of Bcl-2, survivin and significant activation of caspase-3, and its downstream target PARP. These findings provide the rationale for further in vivo and clinical investigation of costunolide against human bladder cancer.
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title_short	Induction of Apoptosis by Costunolide in Bladder Cancer Cells is Mediated through ROS Generation and Mitochondrial Dysfunction
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