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Cancer: Neuroblastoma

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Total 288 results found since Jan 2013.

GSE95057 Exploring the landscape of transcriptome 3 ’ end diversity (TREND) by applying TRENDseq
Conclusions: We analyzed the diversity of the transcriptome 3’end in response to depletion of 174 potential TREND regulators by RNAi. TRENDseq is capable to deconvolute the dynamics of TREND from highly multiplexed libraries. The screening revealed regulators of various l evels of gene expression control (e.g. transcription, splicing, mRNA turnover, etc.) to play an important role in the diversification of the transcriptome 3’ end, affecting over 3600 genes altogether. Data types: 1 – 198 siRNA depletion experiments including 174 knockdowns of putative TREND r egulators and 24 mock control samples. 2 – Biological...
Source: GEO: Gene Expression Omnibus - December 14, 2018 Category: Genetics & Stem Cells Tags: Expression profiling by high throughput sequencing Other Homo sapiens Source Type: research

Nuclear RXRα and RXRβ receptors exert distinct and opposite effects on RA-mediated neuroblastoma differentiation
Publication date: Available online 7 December 2018Source: Biochimica et Biophysica Acta (BBA) - Molecular Cell ResearchAuthor(s): Carolina Saibro Girardi, Diana Carolina Rostirolla, Fernanda Janini Mota Lini, Pedro Ozorio Brum, Jeferson Delgado, Camila Tiefensee Ribeiro, Alexsander Alves Teixeira, Daniel Oppermann Peixoto, Luana Heimfarth, Alice Kunzler, José Cláudio Fonseca Moreira, Daniel Pens GelainAbstractRetinoic acid (RA) promotes differentiation in multiple neurogenic cell types by promoting gene reprogramming through retinoid receptors and also by inducing cytosolic signaling events. The nuclear RXR receptors are...
Source: Biochimica et Biophysica Acta (BBA) Molecular Cell Research - December 7, 2018 Category: Molecular Biology Source Type: research

Mild Hypothermia Prevents NO-Induced Cytotoxicity in Human Neuroblastoma Cells Via Induction of COX-2
AbstractThe cold-inducible protein RBM3 mediates hypothermic neuroprotection against nitric oxide (NO)-induced cell death. Meanwhile, it is well-known that cyclooxygenase-2 (COX-2) is upregulated by RBM3 in several types of cells; however, it is still unclear whether COX-2 contributes to the neuroprotective effects of mild hypothermia/RBM3 against NO-induced cell death. Using human SH-SY5Y neuroblastoma cells, it was revealed that NO remarkably downregulates the expression of COX-2 at both mRNA and protein levels. When COX-2 was silenced using siRNA technique, cells became more sensitive to NO-induced cell death. Conversel...
Source: Journal of Molecular Neuroscience - November 23, 2018 Category: Neuroscience Source Type: research

GSE113734 Loss of the Chr16p11.2 candidate gene QPRT leads to aberrant neuronal differentiation
Conclusions: In this study QPRT was causally related to in vitro neuronal differentiation and affected the regulation of genes and gene-networks that were previously implicated in ASD. Thus, our data suggest that QPRT may play an important role in the pathogenesis of ASD in Chr16p11.2 deletion carriers.
Source: GEO: Gene Expression Omnibus - November 20, 2018 Category: Genetics & Stem Cells Tags: Expression profiling by high throughput sequencing Homo sapiens Source Type: research

Integrated proximal proteomics reveals IRS2 as a determinant of cell survival in ALK-driven neuroblastoma
Oncogenic anaplastic lymphoma kinase (ALK) is one of the few druggable targets in neuroblastoma, and therapy resistance to ALK-targeting tyrosine kinase inhibitors (TKIs) comprises an inevitable clinical challenge. Therefore, a better understanding of the oncogenic signaling network rewiring driven by ALK is necessary to improve and guide future therapies. Here, we performed quantitative mass spectrometry–based proteomics on neuroblastoma cells treated with one of three clinically relevant ALK TKIs (crizotinib, LDK378, or lorlatinib) or an experimentally used ALK TKI (TAE684) to unravel aberrant ALK signaling pathway...
Source: Signal Transduction Knowledge Environment - November 20, 2018 Category: Science Authors: Emdal, K. B., Pedersen, A.-K., Bekker-Jensen, D. B., Lundby, A., Claeys, S., De Preter, K., Speleman, F., Francavilla, C., Olsen, J. V. Tags: STKE Research Resources Source Type: news

Integrated proximal proteomics reveals IRS2 as a determinant of cell survival in ALK-driven neuroblastoma.
Abstract Oncogenic anaplastic lymphoma kinase (ALK) is one of the few druggable targets in neuroblastoma, and therapy resistance to ALK-targeting tyrosine kinase inhibitors (TKIs) comprises an inevitable clinical challenge. Therefore, a better understanding of the oncogenic signaling network rewiring driven by ALK is necessary to improve and guide future therapies. Here, we performed quantitative mass spectrometry-based proteomics on neuroblastoma cells treated with one of three clinically relevant ALK TKIs (crizotinib, LDK378, or lorlatinib) or an experimentally used ALK TKI (TAE684) to unravel aberrant ALK signa...
Source: Science Signaling - November 20, 2018 Category: Biomedical Science Authors: Emdal KB, Pedersen AK, Bekker-Jensen DB, Lundby A, Claeys S, De Preter K, Speleman F, Francavilla C, Olsen JV Tags: Sci Signal Source Type: research

Loss of the Chr16p11.2 ASD candidate gene QPRT leads to aberrant neuronal differentiation in the SH-SY5Y neuronal cell model
ConclusionsIn this study,QPRT was causally related to in vitro neuronal differentiation of SH-SY5Y cells and affected the regulation of genes and gene networks previously implicated in ASD. Thus, our data suggest thatQPRT may play an important role in the pathogenesis of ASD in Chr16p11.2 deletion carriers.
Source: Molecular Autism - November 6, 2018 Category: Molecular Biology Source Type: research

Knockdown of galectin-1 facilitated cisplatin sensitivity by inhibiting autophagy in neuroblastoma cells
In conclusion, galectin-1 knockdown enhanced cisplatin sensitivity of neuroblastoma cells by inhibiting autophagy. The findings might provid a novel therapeutic target to overcome cisplatin resistance in chemotherapy of NB.
Source: Chemico Biological Interactions - October 24, 2018 Category: Biochemistry Source Type: research

Knockdown of galectin-1 facilitated cisplatin sensitivity by inhibiting autophagy in neuroblastoma cells.
In conclusion, galectin-1 knockdown enhanced cisplatin sensitivity of neuroblastoma cells by inhibiting autophagy. The findings might provid a novel therapeutic target to overcome cisplatin resistance in chemotherapy of NB. PMID: 30365942 [PubMed - as supplied by publisher]
Source: Chemico-Biological Interactions - October 23, 2018 Category: Molecular Biology Authors: Gao J, Wang W Tags: Chem Biol Interact Source Type: research

Lentivirus-mediated siRNA knockdown of SPHK1 inhibits proliferation and tumorigenesis of neuroblastoma
Source: OncoTargets and Therapy - October 17, 2018 Category: Cancer & Oncology Tags: OncoTargets and Therapy Source Type: research

Investigation of PP2A and Its Endogenous Inhibitors in Neuroblastoma Cell Survival and Tumor Growth.
In conclusion, activation of PP2A may provide a novel therapeutic target for neuroblastoma. PMID: 30286326 [PubMed - as supplied by publisher]
Source: Translational Oncology - October 1, 2018 Category: Cancer & Oncology Authors: Williams AP, Garner EF, Waters AM, Stafman LL, Aye JM, Markert H, Stewart JE, Beierle EA Tags: Transl Oncol Source Type: research

Tocopherol suppresses 24(S)-hydroxycholesterol-induced cell death via inhibition of CaMKII phosphorylation.
Abstract Although 24(S)-hydroxycholesterol (24S-OHC) plays an important role to maintain homeostasis of cholesterol in the brain, it induces neuronal cell death at high concentrations. 24S-OHC-induced cell death was suppressed by γ-tocopherol (γ-Toc) but not by γ-tocotrienol (γ-Toc3) in a similar way to α-tocopherol (α-Toc) and α-tocotrienol (α-Toc3) in human neuroblastoma SH-SY5Y cells. Both γ-Toc and γ-Toc3 significantly inhibited cumene hydroperoxide-induced cell death, as previously shown in the case of α-Toc and α-Toc3. Lipid droplet-like structure formation induced by 24S-OHC was suppressed by ne...
Source: Biochimie - September 26, 2018 Category: Biochemistry Authors: Kimura Y, Asa M, Urano Y, Saito Y, Nishikawa K, Noguchi N Tags: Biochimie Source Type: research

DUSP5 expression associates with poor prognosis in human neuroblastoma.
Abstract Regulation of growth and differentiation of neuroblastoma (NB) cells is the rational of some maintenance therapies for high-risk NB. MAP kinase phosphatases (MKPs) are potential physiologic regulators of neuronal differentiation and survival, but their expression patterns in NB are scarcely known. Here, an expression analysis of the MKP family has been performed using human NB tumor samples and human NB cell lines (SH-SY5Y, SMS-KCNR, and IMR-32) undergoing retinoic acid (RA)-induced differentiation or subjected to stimuli that activate the MAPK ERK1/2 pathway. We have identified candidate MKPs that could ...
Source: Experimental and Molecular Pathology - August 29, 2018 Category: Pathology Authors: Aurtenetxe O, Zaldumbide L, Erramuzpe A, López R, López JI, Cortés JM, Pulido R, Nunes-Xavier CE Tags: Exp Mol Pathol Source Type: research

Biglycan, a Nitric Oxide-Downregulated Proteoglycan, Prevents Nitric Oxide-Induced Neuronal Cell Apoptosis via Targeting Erk1/2 and p38 Signaling Pathways
AbstractNitric oxide (NO), a gaseous signaling molecule, induces apoptosis and mediates neurodegenerative diseases and brain injury. Biglycan (BGN), a member of the small leucine-rich proteoglycan family, was demonstrated to exert anti-apoptosis function in various disease models. However, little is known about the effect of BGN on NO-induced neurotoxicity. Here, for the first time, we reported that BGN protects against NO-induced apoptosis in human neuroblastoma SH-EP1 cells. This is supported by the finding that sodium nitroprusside (SNP), a NO donor, triggered downregulation of BGN in SH-EP1 cells, and over-expression o...
Source: Journal of Molecular Neuroscience - August 7, 2018 Category: Neuroscience Source Type: research

Heat Shock Protein B8 (HSPB8) Reduces Oxygen-Glucose Deprivation/Reperfusion Injury via the Induction of Mitophagy
Conclusions: HSPB8 promoted OGD/R-induced mitophagy, which restored the mitochondrial function and contributed to the decrease in cell apoptosis after OGD/R. Therefore, HSPB8 could be a favorable neuroprotective agent for cerebral I/R related disorders.Cell Physiol Biochem 2018;48:1492 –1504
Source: Cellular Physiology and Biochemistry - August 2, 2018 Category: Cytology Source Type: research