Melatonin reduces induction of Bax, caspase and cell death in methamphetamine-treated human neuroblastoma SH-SY5Y cultured cells

Apoptosis, or programmed cell death, is an important mechanism in development and in diverse disease states. The morphological characteristics of apoptosis were first identified using the electron microscope. Since then, DNA laddering on agarose gels was found to correlate well with apoptotic cell death in cultured cells of dissimilar origins. Recently numerous DNA nick end labeling methods have been developed in an attempt to visualize, at the light microscopic level, the apoptotic cells responsible for DNA laddering.The present studies were designed to compare various tissue processing techniques and staining methods to assess the occurrence of apoptosis in post mortem tissue from Alzheimer's diseased (AD) and control human brains by DNA nick end labeling methods. Three tissue preparation methods and two commercial DNA nick end labeling kits were evaluated: the Apoptag kit from Oncor and the Biotin-21 dUTP 3' end labeling kit from Clontech. The detection methods of the two kits differed in that the Oncor kit used digoxigenin dUTP and anti-digoxigenin-peroxidase and the Clontech used biotinylated dUTP and avidinperoxidase. Both used 3-3' diaminobenzidine (DAB) for final color development.

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Inhibition of T-type Ca2+ channel induces human neuroblastoma cell death and enhances neurotoxicity of bupivacaine

10.26226/morressier.58f5b031d462b80296c9d36c ◽

2017 ◽

Author(s):

Kumiko Tanaka

Keyword(s):

Cell Death ◽

Neuroblastoma Cell ◽

Human Neuroblastoma Cell ◽

Human Neuroblastoma

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Restricted growth of attenuated poliovirus strains in cultured cells of a human neuroblastoma.

Journal of Virology ◽

10.1128/jvi.63.9.4034-4038.1989 ◽

1989 ◽

Vol 63 (9) ◽

pp. 4034-4038 ◽

Cited By ~ 52

Author(s):

V I Agol ◽

S G Drozdov ◽

T A Ivannikova ◽

M S Kolesnikova ◽

M B Korolev ◽

...

Keyword(s):

Cultured Cells ◽

Human Neuroblastoma

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4-Hydroxychalcone Induces Cell Death via Oxidative Stress in MYCN-Amplified Human Neuroblastoma Cells

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/1670759 ◽

2019 ◽

Vol 2019 ◽

pp. 1-16 ◽

Cited By ~ 2

Author(s):

Amnah M. Alshangiti ◽

Eszter Tuboly ◽

Shane V. Hegarty ◽

Cathal M. McCarthy ◽

Aideen M. Sullivan ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Cell Death ◽

Cytotoxic Effect ◽

Neuroblastoma Cells ◽

Reactive Oxygen ◽

Prognostic Indicator ◽

Oxygen Species ◽

Human Neuroblastoma Cells ◽

Human Neuroblastoma

Neuroblastoma is an embryonal malignancy that arises from cells of sympathoadrenal lineage during the development of the nervous system. It is the most common pediatric extracranial solid tumor and is responsible for 15% of childhood deaths from cancer. Fifty percent of cases are diagnosed as high-risk metastatic disease with a low overall 5-year survival rate. More than half of patients experience disease recurrence that can be refractory to treatment. Amplification of the MYCN gene is an important prognostic indicator that is associated with rapid disease progression and a poor prognosis, highlighting the need for new therapeutic approaches. In recent years, there has been an increasing focus on identifying anticancer properties of naturally occurring chalcones, which are secondary metabolites with variable phenolic structures. Here, we report that 4-hydroxychalcone is a potent cytotoxin for MYCN-amplified IMR-32 and SK-N-BE (2) neuroblastoma cells, when compared to non-MYCN-amplified SH-SY5Y neuroblastoma cells and to the non-neuroblastoma human embryonic kidney cell line, HEK293t. Moreover, 4-hydroxychalcone treatment significantly decreased cellular levels of the antioxidant glutathione and increased cellular reactive oxygen species. In addition, 4-hydroxychalcone treatment led to impairments in mitochondrial respiratory function, compared to controls. In support of this, the cytotoxic effect of 4-hydroxychalcone was prevented by co-treatment with either the antioxidant N-acetyl-L-cysteine, a pharmacological inhibitor of oxidative stress-induced cell death (IM-54) or the mitochondrial reactive oxygen species scavenger, Mito-TEMPO. When combined with the anticancer drugs cisplatin or doxorubicin, 4-hydroxychalcone led to greater reductions in cell viability than was induced by either anti-cancer agent alone. In summary, this study identifies a cytotoxic effect of 4-hydroxychalcone in MYCN-amplified human neuroblastoma cells, which rationalizes its further study in the development of new therapies for pediatric neuroblastoma.

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A Flavonoid-Rich Extract of Mandarin Juice Counteracts 6-OHDA-Induced Oxidative Stress in SH-SY5Y Cells and Modulates Parkinson-Related Genes

Antioxidants ◽

10.3390/antiox10040539 ◽

2021 ◽

Vol 10 (4) ◽

pp. 539

Author(s):

Santa Cirmi ◽

Alessandro Maugeri ◽

Giovanni Enrico Lombardo ◽

Caterina Russo ◽

Laura Musumeci ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Neurodegenerative Diseases ◽

Dopaminergic Neurons ◽

Specific Interaction ◽

Food Sources ◽

Human Neuroblastoma Cell ◽

Neuroprotective Effects ◽

Human Neuroblastoma ◽

Mandarin Juice

Parkinson’s disease (PD) is a degenerative disorder of the nervous system due to unceasing impairment of dopaminergic neurons situated in the substantia nigra. At present, anti-PD drugs acting on dopamine receptors are mainly symptomatic and have only very limited neuroprotective effects, whereas drugs slowing down neurodegeneration of dopaminergic neurons and deterioration of clinical symptoms are not yet available. Given that, the development of more valuable pharmacological strategies is highly demanded. Comprehensive research on innovative neuroprotective drugs has proven that anti-inflammatory and antioxidant molecules from food sources may prevent and/or counteract neurodegenerative diseases, such as PD. The present study was aimed at the evaluation the protective effect of mandarin juice extract (MJe) against 6-hydroxydopamine (6-OHDA)-induced SH-SY5Y human neuroblastoma cell death. Treatment of differentiated SH-SY5Y cells with 6-OHDA brought cell death, and specifically, apoptosis, which was significantly inhibited by the preincubation with MJe through caspase 3 blockage and the modulation of p53, Bax, and Bcl-2 genes. In addition, it showed antioxidant properties in abiotic models as well as in vitro, where it reduced both reactive oxygen and nitrogen species induced by 6-OHDA, along with restored mitochondrial membrane potential, and prevented the oxidative DNA damage evoked by 6-OHDA. Furthermore, MJe restored the impaired balance of SNCA, LRRK2, PINK1, parkin, and DJ-1 gene levels, PD-related factors, caused by 6-OHDA oxidative stress. Overall, these results indicate that MJe exerts neuroprotective effects against 6-OHDA-induced cell death in SH-SY5Y cells by mechanisms involving both the specific interaction with intracellular pathways and its antioxidant capability. Our study suggests a novel possible strategy to prevent and/or ameliorate neurodegenerative diseases, such as PD.

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Inhibition of autophagy by 3-methyladenine potentiates sulforaphane-induced cell death of BE(2)-C human neuroblastoma cells

Molecular Medicine Reports ◽

10.3892/mmr.2015.3377 ◽

2012 ◽

Vol 12 (1) ◽

pp. 535-542 ◽

Cited By ~ 7

Author(s):

IRENA HORWACIK ◽

MONIKA GAIK ◽

MAŁGORZATA DURBAS ◽

ELŻBIETA BORATYN ◽

GRZEGORZ ZAJĄC ◽

...

Keyword(s):

Cell Death ◽

Neuroblastoma Cells ◽

Human Neuroblastoma Cells ◽

Human Neuroblastoma

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Hydrogen Peroxide Toxicity Induces Ras Signaling in Human Neuroblastoma SH-SY5Y Cultured Cells

Journal of Biomedicine and Biotechnology ◽

10.1155/2010/803815 ◽

2010 ◽

Vol 2010 ◽

pp. 1-4 ◽

Cited By ~ 7

Author(s):

Jirapa Chetsawang ◽

Piyarat Govitrapong ◽

Banthit Chetsawang

Keyword(s):

Hydrogen Peroxide ◽

Cell Viability ◽

Cultured Cells ◽

Neuronal Cells ◽

Competitive Inhibitor ◽

Ras Signaling ◽

Ras Proteins ◽

Human Neuroblastoma ◽

Dependent Signaling Pathway

It has been reported that overproduction of reactive oxygen species occurs after brain injury and mediates neuronal cells degeneration. In the present study, we examined the role of Ras signaling on hydrogen peroxide-induced neuronal cells degeneration in dopaminergic neuroblastoma SH-SY5Y cells. Hydrogen peroxide significantly reduced cell viability in SH-SY5Y cultured cells. An inhibitor of the enzyme that catalyzes the farnesylation of Ras proteins, FTI-277, and a competitive inhibitor of GTP-binding proteins, GDP-beta-S significantly decreased hydrogen peroxide-induced reduction in cell viability in SH-SY5Y cultured cells. The results of this study might indicate that a Ras-dependent signaling pathway plays a role in hydrogen peroxide-induced toxicity in neuronal cells.

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Tissue transglutaminase and apoptosis: sense and antisense transfection studies with human neuroblastoma cells

Molecular and Cellular Biology ◽

10.1128/mcb.14.10.6584-6596.1994 ◽

1994 ◽

Vol 14 (10) ◽

pp. 6584-6596

Author(s):

G Melino ◽

M Annicchiarico-Petruzzelli ◽

L Piredda ◽

E Candi ◽

V Gentile ◽

...

Keyword(s):

Cell Death ◽

Structural Changes ◽

Tissue Transglutaminase ◽

Neuroblastoma Cell ◽

Neuroblastoma Cells ◽

Neuroblastoma Cell Line ◽

Human Neuroblastoma Cell ◽

Human Neuroblastoma ◽

Transfected Cells ◽

Protein Levels

In this report, we show that the overexpression of tissue transglutaminase (tTG) in the human neuroblastoma cell line SK-N-BE(2) renders these neural crest-derived cells highly susceptible to death by apoptosis. Cells transfected with a full-length tTG cDNA, under the control of a constitutive promoter, show a drastic reduction in proliferative capacity paralleled by a large increase in cell death rate. The dying tTG-transfected cells exhibit both cytoplasmic and nuclear changes characteristic of cells undergoing apoptosis. The tTG-transfected cells express high Bcl-2 protein levels as well as phenotypic neural cell adhesion molecule markers (NCAM and neurofilaments) of cells differentiating along the neuronal pathway. In keeping with these findings, transfection of neuroblastoma cells with an expression vector containing segments of the human tTG cDNA in antisense orientation resulted in a pronounced decrease of both spontaneous and retinoic acid (RA)-induced apoptosis. We also present evidence that (i) the apoptotic program of these neuroectodermal cells is strictly regulated by RA and (ii) cell death by apoptosis in the human neuroblastoma SK-N-BE(2) cells preferentially occurs in the substrate-adherent phenotype. For the first time, we report here a direct effect of tTG in the phenotypic maturation toward apoptosis. These results indicate that the tTG-dependent irreversible cross-linking of intracellular protein represents an important biochemical event in the induction of the structural changes featuring cells dying by apoptosis.

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TAMI-62. METHIONINE METABOLISM CLOSELY RELATED WITH SELF-RENEW, PLURIPOTENCY AND CELL DEATH IN GICS THROUGH MODIFICATION OF CHOLESTEROL BIOSYNTHESIS, RIBOSOMAL RNA AND AUTOPHAGY

Neuro-Oncology ◽

10.1093/neuonc/noab196.844 ◽

2021 ◽

Vol 23 (Supplement_6) ◽

pp. vi211-vi211

Author(s):

Kiyotaka Yokogami ◽

Hideo Takeshima

Keyword(s):

Stem Cells ◽

Cell Death ◽

Ribosomal Rna ◽

Cell Activation ◽

Cultured Cells ◽

Cholesterol Metabolism ◽

Cholesterol Biosynthesis ◽

Dna Demethylation ◽

Methionine Metabolism ◽

Starting Point

Abstract Glioma initiating cells (GICs) are the source of glioma cells that have the ability to self-renew and pluripotency, which are treatment-resistant, starting point for relapse and eventual death despite multimodality therapy. Since high accumulation is observed in 11cMet-PET at the time of recurrence, it is important to understand the mechanism of tumor cell activation caused by the reorganization of methionine metabolism. We cultured cells in methionine-deprived culture medium and performed a comprehensive analysis, and found that methionine depletion markedly decreased proliferation and increasing cell death of GICs. Decreased SAM, which is synthesized intracellularly catalyzed by methionine adenosyltransferase (MAT) using methionine, triggered the following: (i) global DNA demethylation, (ii) hyper-methylation of signaling pathways regulating pluripotentcy of stem cells, (iii) decreased expression of the core-genes and pluripotent marker of stem cells, (iv) decreased cholesterol synthesis and increased excretion mainly through decreased SREBF2 and FOXM1, (v) down-regulation of the large subunit of ribosomal protein configured 28S and ACA43, snoRNA guiding the pseudouridylation of 28S ribosomal RNA, which has crucial role for translation and (vi) possible connection between methionine metabolism and pluripotency, protein synthesis through cholesterol metabolism: SREBF2-FOXM1 and ACA43 axis, respectively. (vii) Disruption of autophagy by insufficient formation of macroautophagosomes. In conclusion, methionine metabolism closely related with self-renew, pluripotency and cell death in GICs through modification of cholesterol biosynthesis, ribosomal RNA and autophagy.

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