Palmitic acid stimulates energy metabolism and inhibits insulin/PI3K/AKT signaling in differentiated human neuroblastoma cells: The role of mTOR activation and mitochondrial ROS production

2017 ◽  
Vol 110 ◽  
pp. 75-83 ◽  
Author(s):  
Erika Calvo-Ochoa ◽  
Karina Sánchez-Alegría ◽  
Cecilia Gómez-Inclán ◽  
Patricia Ferrera ◽  
Clorinda Arias
Keyword(s):  
Energy Metabolism ◽  
Palmitic Acid ◽  
Neuroblastoma Cells ◽  
Akt Signaling ◽  
Ros Production ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
Mitochondrial Ros

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

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
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