Generation and metabolism of Ins(1,4,5)P3 in SH-SY5Y human neuroblastoma cells: The regulatory role of Ca2+

1991 ◽  
Vol 19 (4) ◽  
pp. 424S-424S ◽  
Author(s):  
DAVID G. LAMBERT ◽  
RICHARD J. H. WOJCIKIEWICZ ◽  
STEFAN R. NAHORSKI
Keyword(s):  
Neuroblastoma Cells ◽  
Regulatory Role ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

Role of the mitochondrial Ca2+ uniporter in Pb2+-induced oxidative stress in human neuroblastoma cells

2014 ◽  
Vol 1575 ◽  
pp. 12-21 ◽  
Author(s):  
Xinyi Yang ◽  
Bin Wang ◽  
Hongqiang Zeng ◽  
Chunqing Cai ◽  
Qiansheng Hu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuroblastoma Cells ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

scholarly journals Repression of BIRC5/Survivin by FOXO3/FKHRL1 Sensitizes Human Neuroblastoma Cells to DNA Damage-induced Apoptosis

2009 ◽  
Vol 20 (7) ◽  
pp. 2041-2048 ◽  
Author(s):  
Petra Obexer ◽  
Judith Hagenbuchner ◽  
Thomas Unterkircher ◽  
Nora Sachsenmaier ◽  
Christoph Seifarth ◽  
...  
Keyword(s):  
Nuclear Translocation ◽  
Chemotherapy Resistance ◽  
Neuroblastoma Cells ◽  
Phosphatidylinositol 3 Kinase ◽  
Human Neuroblastoma Cells ◽  
Hairpin Rna ◽  
Human Neuroblastoma ◽  
Dna Damaging Agents ◽  
Induced Apoptosis

The phosphatidylinositol 3-kinase (PI3K)–protein kinase B (PKB) pathway regulates survival and chemotherapy resistance of neuronal cells, and its deregulation in neuroblastoma (NB) tumors predicts an adverse clinical outcome. Here, we show that inhibition of PI3K-PKB signaling in human NB cells induces nuclear translocation of FOXO3/FKHRL1, represses the prosurvival protein BIRC5/Survivin, and sensitizes to DNA-damaging agents. To specifically address whether FKHRL1 contributes to Survivin regulation, we introduced a 4-hydroxy-tamoxifen-regulated FKHRL1(A3)ERtm allele into NB cells. Conditional FKHRL1 activation repressed Survivin transcription and protein expression. Transgenic Survivin exerted a significant antiapoptotic effect and prevented the accumulation of Bim and Bax at mitochondria, the loss of mitochondrial membrane potential as well as the release of cytochrome c during FKHRL1-induced apoptosis. In concordance, Survivin knockdown by retroviral short hairpin RNA technology accelerated FKHRL1-induced apoptosis. Low-dose activation of FKHRL1 sensitized to the DNA-damaging agents doxorubicin and etoposide, whereas the overexpression of Survivin diminished FKHRL1 sensitization to these drugs. These results suggest that repression of Survivin by FKHRL1 facilitates FKHRL1-induced apoptosis and sensitizes to cell death induced by DNA-damaging agents, which supports the central role of PI3K-PKB-FKHRL1 signaling in drug resistance of human NB.

scholarly journals The essential role of ERK in 4-oxo-2-nonenal-mediated cytotoxicity in SH-SY5Y human neuroblastoma cells

2009 ◽  
Vol 108 (6) ◽  
pp. 1434-1441 ◽  
Author(s):  
Hyun-Pil Lee ◽  
Xiaochun Zhu ◽  
Xiongwei Zhu ◽  
S. Chad Skidmore ◽  
George Perry ◽  
...  
Keyword(s):  
Essential Role ◽  
Neuroblastoma Cells ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

scholarly journals Role of genomic architecture in the expression dynamics of long noncoding RNAs during differentiation of human neuroblastoma cells

2013 ◽  
Vol 7 (Suppl 3) ◽  
pp. S11 ◽  
Author(s):  
Arsen O Batagov ◽  
Aliaksandr A Yarmishyn ◽  
Piroon Jenjaroenpun ◽  
Jovina Z Tan ◽  
Yuichiro Nishida ◽  
...  
Keyword(s):  
Neuroblastoma Cells ◽  
Noncoding Rnas ◽  
Long Noncoding Rnas ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
Genomic Architecture

Apoptosis Induced in T Cells by Human Neuroblastoma Cells: Role of Fas Ligand

1998 ◽  
Vol 16 (5-6) ◽  
pp. 263-274 ◽  
Author(s):  
Galina V. Shurin ◽  
Valentin Gerein ◽  
Michael T. Lotze ◽  
Edward M. Barksdale Jr.
Keyword(s):  
T Cells ◽  
Fas Ligand ◽  
Neuroblastoma Cells ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

scholarly journals Stimulatory Heterotrimeric GTP-binding Protein Inhibits Hydrogen Peroxide-induced Apoptosis by Repressing BAK Induction in SH-SY5Y Human Neuroblastoma Cells

2007 ◽  
Vol 283 (3) ◽  
pp. 1350-1361 ◽  
Author(s):  
So-Young Kim ◽  
MiRan Seo ◽  
Yeni Kim ◽  
Yun-Il Lee ◽  
Jung-Min Oh ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Cancer Cells ◽  
Neuroblastoma Cells ◽  
Camp Signaling ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
Gtp Binding ◽  
Camp Signaling Pathway ◽  
Induced Apoptosis

Heterotrimeric stimulatory GTP-binding protein (Gs) stimulates adenylate cyclases to activate the cAMP signaling pathway. Although the cAMP pathway has been reported to be involved in apoptosis, the role of the Gs-cAMP signaling pathway during reactive oxygen species (ROS)-mediated apoptosis, which is involved in the resistance of cancer cells to chemotherapy and radiation, is not clearly understood. Thus, in this study we aimed to investigate the role of the α subunit of Gs (Gαs) in the ROS-induced apoptosis of cancer cells. The stable expression of constitutively active Gαs (GαsQL) inhibited the hydrogen peroxide-induced apoptosis of SH-SY5Y human neuroblastoma cells and reduced the hydrogen peroxide-induced increase in Bak and the decrease in Bcl-xL protein expression. Exogenous Bak expression abolished these inhibitory effects of GαsQL, but Bak small interfering RNA decreased hydrogen peroxide-induced apoptosis. Gαs repressed hydrogen peroxide-induced Bak expression by inhibiting the transcription of Bak mRNA, which resulted from the inhibition of the hydrogen peroxide-induced activation of transcription factors such as AP1, NF-κB, and NFAT. Moreover, Gαs also inhibited the hydrogen peroxide-induced binding of AP1, NF-κB, and NFAT to the Bak promoter. Furthermore, hydrogen peroxide-induced apoptosis was reduced by treating cells with prostaglandin E2, which activates Gαs, but this was augmented by CCPA, which activates Gαi causing a decrease in cAMP levels. From the results, we conclude that Gαs protects neuroblastoma cells from hydrogen peroxide-induced apoptosis by repressing Bak induction, which is mediated by the inhibition of the hydrogen peroxide-induced activations of AP1, NF-κB, and NFAT through cAMP-PKA-CREB signaling system.

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