Activation of caspases and cleavage of Bid are required for tyrosine and phenylalanine deficiency-induced apoptosis of human A375 melanoma cells

Ge, Xiaokang; Fu, Yiming; Li, Yiqi; Meadows, Gary G.

doi:10.1016/s0003-9861(02)00211-4

Cited by 11 publications

(17 citation statements)

References 36 publications

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“…4). Deprivation of essential amino acids can act as apoptotic trigger, as shown in human A375 melanoma cells grown in tyrosine and phenylalanine-free medium, [43] however apoptosis is delayed compared to the effect induced by LAAO. In the latter case, 70% of the cells became apoptotic within 24 h while only 33% apoptosis was observed after 72 h incubation under tyrosine and phenylalanine-free conditions.…”

Section: Discussionmentioning

confidence: 98%

Mechanisms of cell death induction by L-amino acid oxidase, a major component of ophidian venom

et al. 2006

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L-amino acid oxidase (LAAO) from the Malayan pit viper induces both necrosis and apoptosis in Jurkat cells. Cell death by necrosis is attributed to H 2 O 2 produced by oxidation of α-amino acids. In the presence of catalase that effectively scavenges H 2 O 2, a switch to apoptosis is observed. The major factors contributing to apoptosis are proposed to be: (i) generation of toxic intermediates from fetal calf serum (ii) binding and internalization of LAAO. The latter process appears to be mediated by the glycan moiety of the enzyme as desialylation reduces cytotoxicity. D-amino acid oxidase (DAAO), which catalyzes the same reaction as LAAO but lacks glycosylation, triggers necrosis as a consequence of H 2 O 2 production but not apoptosis in the presence of catalase. Thus induction of cell death by LAAO appears to involve both the generation of H 2 O 2 and the molecular interaction of the glycan moiety of the enzyme with structures at the cell surface.S. R. Ande, P. R. Kommoju contributed equally to this work.

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Section: Discussionmentioning

confidence: 98%

Mechanisms of cell death induction by L-amino acid oxidase, a major component of ophidian venom

et al. 2006

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“…It is known from animal studies that RTEs exiting the thymus initially home to lymph nodes, and that expansion of these cells is likely to occur at sites of IL-7 production such as skin, gut, and the liver. Paradoxically, these organs through the presence of macrophages and immature dendritic cells expressing CD95L (45,46) could also provide a mechanism for limiting the expansion of immature RTEs in the periphery. Although the need for restriction of Ag-independent cell expansion under normal physiological conditions may be limited, it is, however, likely to be an important mechanism to prevent uncontrolled bystander T cell expansion in lymphoid tissues as part of the adaptive immune response.…”

Section: Discussionmentioning

confidence: 99%

IL-7-Regulated Homeostatic Maintenance of Recent Thymic Emigrants in Association with Caspase-Mediated Cell Proliferation and Apoptotic Cell Death

O’Neill

Hassan

Reen

2003

The Journal of Immunology

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Homeostasis of T cells is essential to the maintenance of the T cell pool and TCR diversity. In this study, mechanisms involved in the regulation of cytokine-mediated expansion of naive T cells in the absence of Ag, in particular the role of caspase activation and susceptibility to apoptosis of recent thymic emigrants (RTEs), were examined. Low level caspase-8 and caspase-3 activation was detected in proliferating IL-7-treated cells in the absence of cell death during the first days of culture. Caspase inhibitors suppressed IL-7-induced expansion of RTEs. Low level expression of CD95 and blocking Ab experiments indicated that this early caspase activation was CD95 independent. However, CD95 levels subsequently became dramatically up-regulated on proliferating naive T cells, and these cells became susceptible to CD95 ligation, resulting in high level caspase activation and apoptotic cell death. These results show a dual role for caspases in proliferation and in CD95-induced cell death during Ag-independent expansion of RTEs. This method of cell death in IL-7-expanded RTEs is a previously unrecognized mechanism for the homeostatic control of expanded T cells.

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“…However, neither of the restrictions induces apoptosis of normal prostate epithelial cells (Fu et al, 2003). We found that apoptosis induced by specific amino acid restriction is a relatively slow process (Fu et al, , 2003Ballif and Blenis, 2001;Ge et al, 2002). Raf and Akt are major survival pathways in mammalian cells; inhibition of these pathways results in slow cell death (Ballif and Blenis, 2001;Green and Evans, 2002).…”

mentioning

confidence: 89%

“…The caspase inhibitor, Z.VAD.fmk (CalBiochem, San Diego, CA) at 10 mM, or decylubiquinone ((DUN), Sigma, St. Louis, MO), an inhibitor of the mitochondria permeability transition pore, at 50 mM was added into the medium of some experiments. These concentrations were based on previous experiments (Ge et al, 2002). All experiments were repeated at least three times.…”

Section: Cell Culture Conditionsmentioning

confidence: 99%

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Selective amino acid restriction targets mitochondria to induce apoptosis of androgen‐independent prostate cancer cells

Zhang

Ding

et al. 2006

Journal Cellular Physiology

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Relative specific amino acid dependency is one of the metabolic abnormalities of cancer cells, and restriction of specific amino acids induces apoptosis of prostate cancer cells. This study shows that restriction of tyrosine and phenylalanine (Tyr/Phe), glutamine (Gln), or methionine (Met), modulates Raf and Akt survival pathways and affects the function of mitochondria in DU145 and PC3, in vitro. These three restrictions inhibit energy production (ATP synthesis) and induce generation of reactive oxygen species (ROS). Restriction of Tyr/Phe or Met in DU145 and Met in PC3 reduces mitochondrial membrane potential (DeltaPsim) and induces caspase-dependent and -independent apoptosis. In DU145, Tyr/Phe or Met restriction reduces activity of Akt, mitochondrial distribution of phosphorylated Raf and apoptosis inducing factor (AIF), and increases mitochondrial distribution of Bak. Mitochondrial Bcl-XL is increased in Tyr/Phe-restricted but decreased in Met-restricted cells. Under Tyr/Phe or Met restriction, reduced mitochondrial Raf does not inactivate the pro-apoptotic function of Bak. Tyr/Phe restriction also inhibits Bcl-2 and Met restriction inhibits Bcl-XL in mitochondria. These comprehensive actions damage the integrity of the mitochondria and induce apoptosis of DU145. In PC3, apoptosis induced by Met restriction was not associated with alterations in intracellular distribution of Raf, Bcl-2 family proteins, or AIF. All of the amino acid restrictions inhibited Akt activity in this cell line. We conclude that specific amino acid restriction differentially interferes with homeostasis/balance between the Raf and Akt survival pathways and with the interaction of Raf and Bcl-2 family proteins in mitochondria to induce apoptosis of DU145 and PC3 cells.

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Activation of caspases and cleavage of Bid are required for tyrosine and phenylalanine deficiency-induced apoptosis of human A375 melanoma cells

Cited by 11 publications

References 36 publications

Mechanisms of cell death induction by L-amino acid oxidase, a major component of ophidian venom

Mechanisms of cell death induction by L-amino acid oxidase, a major component of ophidian venom

IL-7-Regulated Homeostatic Maintenance of Recent Thymic Emigrants in Association with Caspase-Mediated Cell Proliferation and Apoptotic Cell Death

Selective amino acid restriction targets mitochondria to induce apoptosis of androgen‐independent prostate cancer cells

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