Pathways to caspase activation

Wang, Zi-Bing; Liu, Yuqing; Cui, Yan

doi:10.1016/j.cellbi.2005.04.001

Cited by 184 publications

(143 citation statements)

References 97 publications

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“…Ultimately it leads to the activation of caspase-9. Cleaved or active form of caspase-9 cleaves effector caspases including caspase-3, -6, and also -7 (Wang et al 2005). The current study demonstrated that DAM and NDAM-treated H400 OSCC cells exhibited an increase in the activity of Cytochrome c, caspase-9 and also caspase-3/7.…”

Section: Discussionsupporting

confidence: 58%

Cell cycle arrest and mechanism of apoptosis induction in H400 oral cancer cells in response to Damnacanthal and Nordamnacanthal isolated from Morinda citrifolia

et al. 2016

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Oral cancer is the eleventh most prevalent cancer worldwide. The most prevalent oral cancer is oral squamous cell carcinoma (OSCC). Damnacanthal (DAM) and nordamnacanthal (NDAM), the anthraquinone compounds, are isolated from the root of Morinda citrifolia L. (Noni), which has been used for the treatment of several chronic diseases including cancer. The objectives of this study were to evaluate the cytotoxicity, cell death mode, cell cycle, and the molecular mechanism of apoptosis induced by DAM and NDAM on OSCC. The cytotoxic effects of these compounds against OSCC cell lines were determined by MTT assay. The cell death mode was analysed by DNA laddering and FITC-annexin V/PI flow cytometric assays. In addition, the mechanism of apoptosis induced by DAM and NDAM was detected using mitochondrial membrane potential, Cytochrome c, and caspases assays. Finally, the effect of DAM and NDAM on cell cycle phase distribution of OSCC cells was detected by flow cytometry. In the present study, DAM and NDAM showed cytotoxicity towards OSCC cell lines and the maximum growth inhibition for both compounds was observed in H400 cells with IC 50 value of 1.9 and 6.8 lg/ml, respectively, after 72 h treatment. The results also demonstrated the inhibition of H400 OSCC cells proliferation, internucleosomal cleavage of DNA, activation of intrinsic apoptosis pathway, and cell cycle arrest caused by DAM and NDAM. Therefore, these findings suggest that DAM and NDAM can be potentially used as antitumor agents for oral cancer therapy.

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Section: Discussionsupporting

confidence: 58%

Cell cycle arrest and mechanism of apoptosis induction in H400 oral cancer cells in response to Damnacanthal and Nordamnacanthal isolated from Morinda citrifolia

et al. 2016

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“…1) [22]. The extrinsic apoptotic signaling is initiated by death receptors located on the cell surface, such as the tumor necrosis factor receptor (TNF-R) and the Fas receptor [24]. Activation of these receptors by binding of death-stimulating ligands results in the recruitment of adaptor proteins, such as Fas-associated death domain (FADD), TNF-receptor-associated death domain (TRADD), and TNF-receptor-associated factors (TRAFs), forming the death-inducing signaling complex (DISC), which engages and activates procaspase-8.…”

Section: Signaling Pathways Of Apoptotic Cell Deathmentioning

confidence: 99%

“…Activation of these receptors by binding of death-stimulating ligands results in the recruitment of adaptor proteins, such as Fas-associated death domain (FADD), TNF-receptor-associated death domain (TRADD), and TNF-receptor-associated factors (TRAFs), forming the death-inducing signaling complex (DISC), which engages and activates procaspase-8. Active caspase-8 subsequently activates caspase-3 [24]. Intrinsic pathways of caspase activation include those triggered by the endoplasmic reticulum (ER) and the mitochondrion [22].…”

Section: Signaling Pathways Of Apoptotic Cell Deathmentioning

confidence: 99%

Multiple Pathways to the Same End: Mechanisms of Myonuclear Apoptosis in Sarcopenia of Aging

Marzetti

Privitera

Simili

et al. 2010

The Scientific World JOURNAL

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Sarcopenia, the age-related decline in muscle mass and function, represents a significant health issue due to the high prevalence of frailty and disability associated with this condition. Nevertheless, the cellular mechanisms responsible for the loss of muscle mass in old age are still largely unknown. An altered regulation of myocyte apoptosis has recently emerged as a possible contributor to the pathogenesis of sarcopenia. Studies in animal models have shown that the severity of skeletal muscle apoptosis increases over the course of aging and correlates with the degree of muscle mass and strength decline. Several apoptotic pathways are operative in aged muscles, with the mitochondria- and TNF-α-mediated pathways likely being the most relevant to sarcopenia. However, despite the growing number of studies on the subject, a definite mechanistic link between myocyte apoptosis and age-related muscle atrophy has not yet been established. Furthermore, the evidence on the role played by apoptosis in human sarcopenia is still sparse. Clearly, further research is required to better define the involvement of myocyte apoptosis in the pathogenesis of muscle loss at advanced age. This knowledge will likely help in the design of more effective therapeutic strategies to preserve muscle mass into old age, thus fostering independence of the elderly population and reducing the socioeconomic burden associated with sarcopenia.

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“…Morphological changes in the nucleus include condensation/margination of chromatin, DNA fragmentation in a laddering pattern, and nuclear fragmentation. Apoptotic cells are also characterized by the externalization of phosphatidyl-serine (PS), cell shrinkage, membrane blebbing, a peculiar boiling action of the plasma membrane (zeiosis), and fragmentation of the cell into apoptotic bodies (Vermeulen et al, 2005;Wang et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Diepoxybutane activates the mitochondrial apoptotic pathway and mediates apoptosis in human lymphoblasts through oxidative stress

Yadavilli¹,

Martinez‐Ceballos²,

Snowden-Aikens³

et al. 2007

Toxicology in Vitro

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Diepoxybutane (DEB) is the most potent metabolite of the environmental chemical 1, 3-butadiene (BD), which is prevalent in petrochemical industrial areas. BD is a known mutagen and human carcinogen, and possesses multi-systems organ toxicity. We recently reported that DEB-induced cell death in TK6 lymphoblasts was due to the occurrence of apoptosis, and not necrosis. In this study, we investigated the molecular mechanisms responsible for DEB-induced apoptosis in these cells. Bax and Bak were found to be over-expressed and activated, and the mitochondrial trans-membrane potential was attenuated in cells undergoing DEB-induced apoptosis. Cytochrome c was depleted from the mitochondria of TK6 cells undergoing apoptosis, and was released into the cytosol in Jurkat-T lymphoblasts exposed to the same concentrations of DEB. Executioner caspase 3 was deduced to be activated by initiator caspase 9. DEB induced reactive oxygen species (ROS) formation, and the ROS scavenger N-acetyl-L-cysteine effectively blocked DEB-induced apoptosis in TK6 cells.Collectively, these results demonstrate that the mitochondrial apoptotic pathway is activated to mediate DEB-induced apoptosis in human TK6 lymphoblasts. These results further demonstrate that DEB-induced apoptosis is also mediated by the DEB-induced generation of ROS. This is the first report to examine the mechanism of DEB-induced apoptosis in human lymphoblasts.

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Pathways to caspase activation

Cited by 184 publications

References 97 publications

Cell cycle arrest and mechanism of apoptosis induction in H400 oral cancer cells in response to Damnacanthal and Nordamnacanthal isolated from Morinda citrifolia

Cell cycle arrest and mechanism of apoptosis induction in H400 oral cancer cells in response to Damnacanthal and Nordamnacanthal isolated from Morinda citrifolia

Multiple Pathways to the Same End: Mechanisms of Myonuclear Apoptosis in Sarcopenia of Aging

Diepoxybutane activates the mitochondrial apoptotic pathway and mediates apoptosis in human lymphoblasts through oxidative stress

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