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Open AccessJournal ArticleDOI

Oxidative stress-mediated apoptosis. The anticancer effect of the sesquiterpene lactone parthenolide.

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TLDR
It is found that parthenolide effectively inhibits hepatoma cell growth in a tumor cell-specific manner and triggers apoptosis of hepatoma cells and may be useful chemotherapeutic agents to treat these invasive cancers.
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This article is published in Journal of Biological Chemistry.The article was published on 2002-10-11 and is currently open access. It has received 314 citations till now. The article focuses on the topics: Parthenolide & Apoptosis.

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Signal transduction mediated by the Ras/Raf/MEK/ERK pathway from cytokine receptors to transcription factors: potential targeting for therapeutic intervention

TL;DR: The current understanding of the Ras/Raf/MEK/ERK signal transduction pathway and the downstream transcription factors is summarized and the prospects of targeting this pathway for therapeutic intervention in leukemia and other cancers will be evaluated.
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Sesquiterpenoids Lactones: Benefits to Plants and People

TL;DR: The varied ecological roles of sesquiterpenes in the plant producer, depending upon the plant and the compound are explored, including allelopathy with other plants, insects, and microbes, thereby causing behavioural or developmental modification to these secondary organisms to the benefit of the sesqiterpenoid producer.
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Critical roles of intracellular thiols and calcium in parthenolide-induced apoptosis in human colorectal cancer cells

TL;DR: It is demonstrated that the intracellular thiols and calcium equilibrium play a critical role in parthenolide-induced apoptotic cell death.
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Reactive Oxygen Species Produced by NAD(P)H Oxidase Inhibit Apoptosis in Pancreatic Cancer Cells

TL;DR: The results show that growth factor-induced ROS produced by NAD(P)H oxidase (probably Nox4) protect pancreatic cancer cells from apoptosis, and may play an important role in pancreaticcancer resistance to treatment and thus represent a novel therapeutic target.
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Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease Cascade

TL;DR: Mutation of the active site of caspase-9 attenuated the activation of cazase-3 and cellular apoptotic response in vivo, indicating that casp enzyme-9 is the most upstream member of the apoptotic protease cascade that is triggered by cytochrome c and dATP.
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An Essential Role for NF-κB in Preventing TNF-α-Induced Cell Death

TL;DR: Reintroduction of RelA into RelA−/− fibroblasts resulted in enhanced survival, demonstrating that the presence ofrelA is required for protection from TNF-α.
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NF-κB: Ten Years After

TL;DR: The manuscript and the Figures and Table are based on a manuscript originally written by Gordon C. Dickinson in 2012 and then edited by David I. Dickinson and revised by David A. Dickinson.
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NF-κB Antiapoptosis: Induction of TRAF1 and TRAF2 and c-IAP1 and c-IAP2 to Suppress Caspase-8 Activation

TL;DR: Tumor necrosis factor alpha binding to the TNF receptor (TNFR) potentially initiates apoptosis and activates the transcription factor nuclear factor kappa B (NF-kappaB), which suppresses apoptosis by an unknown mechanism.
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TNF- and Cancer Therapy-Induced Apoptosis: Potentiation by Inhibition of NF-κB

TL;DR: The activation of the transcription factor nuclear factor-kappa B by tumor necrosis factor, ionizing radiation, or daunorubicin, was found to protect from cell killing, providing a mechanism of cellular resistance to killing by some apoptotic reagents.
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