Molecular mechanism of satratoxin-induced apoptosis in HL-60 cells: activation of caspase-8 and caspase-9 is involved in activation of caspase-3

Nagase, Masahiro; Shiota, Tetsuya; Tsushima, Akiko; Alam, Mohammad Murshedul; Fukuoka, Satoshi; Yoshizawa, Takumi; Sakato, Nobuo

doi:10.1016/s0165-2478(02)00127-x

Cited by 32 publications

(18 citation statements)

References 16 publications

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“…In the present study, we showed that satratoxin H (50 nM) increased cleavage of caspase-3, which was mediated through p38 MAPK and/or JNK. Our data were concomitant with the previous studies, in which apoptosis mediated through caspase-3 is induced by other trichothecenes, such as T-2 toxin (Bouaziz et al, 2006), 4-acetyl-12,13-epoxyl-9-trichothecene-3,15-diol (Pae et al, 2003), and satratoxin G (Nagase et al, 2002). Stratoxin G-producing S. chartarum IBT 9631, as well as satratoxin G, increased phosphorylation of p38 MAPK and activation of caspase-3 (Rakkestad et al, 2010).…”

Section: Discussionsupporting

confidence: 90%

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Apoptotic effects of satratoxin H is mediated through DNA double-stranded break in PC12 cells

et al. 2012

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-Satratoxin H is an important air-and food-borne mycotoxin, which has been implicated in human health damage. Satratoxin H is known to induce apoptosis as well as genotoxicity in PC12 cells. In the present study, we further investigated the mechanism of apoptotic effects of satratoxin H with focus on caspase-3 and poly-ADP-ribose polymerase (PARP) pathway. We also examined whether it induces DNA damage in PC12 cells. In the cells treated with satratoxin H, caspase-3 was cleaved in a time-dependent manner. Furthermore, satratoxin H induced cleavage of PARP, one of the downstream molecules of caspase-3. The cleavage was inhibited by SB203580, a p38 MAPK inhibitor, or SP600125, a JNK inhibitor. Satratoxin H, however, had no effect on expression levels of Bax and Bcl-2. Furthermore, the micronucleus assay revealed that satratoxin H induced chromosome break. Also, satratoxin H increased the level of phosphorylation of histone H2A, indicating that it caused DNA double-stranded breaks in PC12 cells. Meanwhile, no genotoxicity was detected with any of treatments carried out in the alkaline comet assay. These results imply that satratoxin H induces genotoxicity by DNA double-stranded break. Our results suggest a considerable potential for the genotoxic risk associated with the presence of satratoxin H.

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Section: Discussionsupporting

confidence: 90%

“…To test genotoxicity, the cells were treated with various concentrations of satratoxin H for 24 hr. After treatment, the whole cell proteins were extracted in lysis buffer (50 mM (Nagase et al, 2002). Vol.…”

Section: Western Blot Analysismentioning

confidence: 99%

Apoptotic effects of satratoxin H is mediated through DNA double-stranded break in PC12 cells

et al. 2012

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“…42 Cytochrome c was the first mitochondrial protein found to participate in the mitochondria-dependent pathway. 43 In theory, caspase-3 is activated through activation of caspase-9 along with cytosolic release of cytochrome c. 44 Results from our TUNEL and Western blot assays demonstrated apoptosis in visible forms, which is consistent with our aforementioned results.…”

Section: Discussionsupporting

confidence: 88%

Immunoliposome co-delivery of bufalin and anti-CD40 antibody adjuvant induces synergetic therapeutic efficacy against melanoma

Li¹,

Yuan²,

Yang³

et al. 2014

IJN

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Liposomes constitute one of the most popular nanocarriers for improving the delivery and efficacy of agents in cancer patients. The purpose of this study was to design and evaluate immunoliposome co-delivery of bufalin and anti-CD40 to induce synergetic therapeutic efficacy while eliminating systemic side effects. Bufalin liposomes (BFL) conjugated with anti-CD40 antibody (anti-CD40-BFL) showed enhanced cytotoxicity compared with bufalin alone. In a mouse B16 melanoma model, intravenous injection of anti-CD40-BFL achieved smaller tumor volume than did treatment with BFL (average: 117 mm 3 versus 270 mm 3 , respectively); the enhanced therapeutic efficacy through a caspase-dependent pathway induced apoptosis, which was confirmed using terminal deoxynucleotidyl transferase-mediated dUTP-Fluorescein nick end labeling and Western blot assay. Meanwhile, anti-CD40-BFL elicited unapparent body-weight changes and a significant reduction in serum levels of tumor necrosis factor-α, interleukin-1β, interleukin-6, interferon-γ, and hepatic enzyme alanine transaminase, suggesting minimized systemic side effects. This may be attributed to the mechanism by which liposomes are retained within the tumor site for an extended period of time, which is supported by the following biodistribution and flow cytometric analyses. Taken together, the results demonstrated a highly promising strategy for liposomal vehicle transport of anti-CD40 plus bufalin that can be used to enhance antitumor effects via synergetic systemic immunity while blocking systemic toxicity.

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“…* pϽ0.05 compared to control cells. signaling pathways, 55) and/or ROS as suggested in the previous study. 14) However, the weak protective effect of GSH in satratoxin H-induced cytotoxicity in our previous report 14) implies that the generation of intracellular ROS may be one of the mechanisms by which satratoxin H induces apoptosis in PC12 cells.…”

Section: )mentioning

confidence: 55%

Satratoxin H Generates Reactive Oxygen Species and Lipid Peroxides in PC12 Cells

Nusuetrong

Pengsuparp

Meksuriyen

et al. 2008

Biological & Pharmaceutical Bulletin

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Satratoxin H, a mycotoxin, is thought to induce apoptosis of PC12 cells through the activation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK) in a glutathione (GSH)-sensitive manner. The present study was undertaken to further elucidate the mechanism by which satratoxin H induces cell death in PC12 cells. Satratoxin H caused apoptosis of PC12 cells within 24-h, as determined by DNA fragmentation and flow cytometric analysis. Satratoxin H increased reactive oxygen species (ROS) production and lipid peroxidation, as determined by malondialdehyde formation. These effects were attenuated by incubation of cells with GSH, suggesting that satratoxin H-induced increase in apoptosis of serum-deprived PC12 cells may be partially mediated through the generation of ROS.

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Molecular mechanism of satratoxin-induced apoptosis in HL-60 cells: activation of caspase-8 and caspase-9 is involved in activation of caspase-3

Cited by 32 publications

References 16 publications

Apoptotic effects of satratoxin H is mediated through DNA double-stranded break in PC12 cells

Apoptotic effects of satratoxin H is mediated through DNA double-stranded break in PC12 cells

Immunoliposome co-delivery of bufalin and anti-CD40 antibody adjuvant induces synergetic therapeutic efficacy against melanoma

Satratoxin H Generates Reactive Oxygen Species and Lipid Peroxides in PC12 Cells

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