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Glycosyl-T expression in NB cells

ABSTRACT: Dr. Ladisch's work focuses on the establishment of the biological significance of gangliosides that are shed by tumor cells, particularly those involved in pediatric cancers, including brain tumors and neuroblastoma. These studies are directed toward illuminating the hypothesis that shed gangliosides enhance tumor formation, possibly both by inhibiting the antitumor immune response and by enhancing growth factor-induced signaling and proliferation of fibrobalsts and vascular endotheilial cells in the tumor microenvironment. Delineation of the signaling pathways affected by ganglioside exposure is currently under study. The effect of retinoic acid on the mRNA levels of ganglioside glycosyltransferases in neuroblastoma cells in vitro Experiment to determine mRNA expression for ganglioside glycosyltransferases in NB cells (untreated versus treated with ATRA) using the Glyco-gene Chip by the Consortium for Functional Glycomics. Human NB cell lines LAN-5 were incubated with 10 µM of all-trans retinoic acid or untreated as control, and total RNA harvested after 24 hours, 72 hours and 120 hours of exposure to retinoic acid. We performed three independent experiments on either cell line so that for each cell line and each time point three replicates were be obtained (total: 18 chips). Glycosyltransferases of particular interest are LacCer synthase, GlucCer synthase, GM3 synthase, GD3 synthase, GM2/GD2 synthase, GD1b/GM1a synthase, GT1b/GD1a synthase and GQ1b/GT1a synthase.

ORGANISM(S): Homo sapiens

SUBMITTER: Steven Head

PROVIDER: E-GEOD-26481 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Glycosyl-T expression in NB cells

Project description:Dr. Ladisch's work focuses on the establishment of the biological significance of gangliosides that are shed by tumor cells, particularly those involved in pediatric cancers, including brain tumors and neuroblastoma. These studies are directed toward illuminating the hypothesis that shed gangliosides enhance tumor formation, possibly both by inhibiting the antitumor immune response and by enhancing growth factor-induced signaling and proliferation of fibrobalsts and vascular endotheilial cells in the tumor microenvironment. Delineation of the signaling pathways affected by ganglioside exposure is currently under study.

2011-01-07 | GSE26481 | GEO

Lamin A/C is required for SHSY5Y neuroblastoma cell differentiation and its expression is linked to a less malignant phenotype.

Project description:The main scientific objective of the project was to investigate whether Lamin A/C could be involved in neuroblastoma differentiation. Moreover, taking into account the significance of differentiation stage in the neuroblastoma tumor progression we have also studied a possible role of Lamin A/C in the tumorigenesis of this neuronal cancer. As differentiating stimulus we used the all-trans retinoic acid (RA), the most effective compound which has been shown to induce differentiation in neuroblastoma cells. To get insight into the impairment of cell differentiation produced by the LMNA (Lamin A/C) silencing in SHSY5Y cells, we compared the gene expression profile of control and silenced cells both in Retinoic Acid treated and untreated samples, using the one-color Agilent microarray platform. Four condition experiment: cells infected with a mock vector (Mock cells), treated and untreated with retinoic acid (RA); cells infected with a silencing vector for LMNA (LMNA-KD cells), treated and untreated with retinoic acid.

2013-07-11 | E-GEOD-30677 | biostudies-arrayexpress

Expression data for developing a GE-HTS signature for neuroblastoma differentiation

Project description:Gene expression data from BE(2)-C cells treated in triplicate with either vehicle (DMSO), 5 M-NM-<M all-trans retinoic acid (ATRA), 1 mM valproic acid (VPA), or 5 M-NM-<M ATRA + 1 mM VPA for 6, 24, or 72 hours. Genome-wide expression profiling was performed using Affymetrix U133A microarrays. While cytotoxic chemotherapy remains the hallmark of cancer treatment, intensive regimens fall short in many malignancies, including high-risk neuroblastoma. One alternative strategy is to therapeutically promote tumor differentiation. We created a gene expression signature to measure neuroblast maturation, adapted it to a high-throughput platform, and screened a diversity oriented synthesis-generated small-molecule library for differentiation inducers. We identified BRD8430, containing a nine-membered lactam, an ortho-amino anilide functionality, and three chiral centers, as a selective Class I histone deacetylase (HDAC) inhibitor (HDAC1 > 2 > 3). Further investigation demonstrated that selective HDAC1/HDAC2 inhibition using compounds or RNA interference induced differentiation and decreased viability in neuroblastoma cell lines. Combined treatment with 13-cis retinoic acid augmented these effects and enhanced activation of retinoic acid signaling. Therefore, by applying a chemical genomic screening approach we identified selective HDAC1/HDAC2 inhibition as a strategy to induce neuroblastoma differentiation. BE(2)-C cells were treated in triplicate with either vehicle (DMSO), 5 M-NM-<M all-trans retinoic acid (ATRA), 1 mM valproic acid (VPA), or 5 M-NM-<M ATRA + 1 mM VPA for 6, 24, or 72 hours. Genome-wide expression profiling was performed using Affymetrix U133A microarrays [HT-HG_U133A Early Access].

2013-04-08 | E-GEOD-45587 | biostudies-arrayexpress

CHAF1A Blocks Neuronal Differentiation and Promotes Neuroblastoma Oncogenesis via Metabolic Reprogramming

Project description:Neuroblastoma (NB) arises from neural crest cells (NCCs) secondary to a block in differentiation. Retinoic acid (RA) differentiation therapy has limited therapeutic efficacy, and the mechanisms preventing terminal differentiation remain elusive. We found that the chromatin modifier CHAF1A restricts neuronal differentiation and promotes NB oncogenesis. CHAF1A blocks NC differentiation into mature neurons in both human NCCs and zebrafish models. CHAF1A gain-of-function promotes cell malignancy, blocks RA-induced differentiation, and is sufficient to induce NB tumor formation. Mechanistically, CHAF1A blocks NB differentiation by repressing gene expression programs promoting neuronal development and differentiation, and rewiring polyamine metabolism. Targeting polyamine synthesis restores NB sensitivity to RA therapy. Our results demonstrate that CHAF1A critically contributes to NB oncogenesis by blocking neuronal differentiation and reprogramming cell metabolism.

2021-07-20 | GSE144311 | GEO

Translatome profiling of neuroblastoma cells CHP134 treated with isotretinoin (13cRA), isorhamnetin (ISR), and their combination

Project description:Neuroblastoma (NB) is an aggressive childhood tumor, with high-risk cases having a 5-year overall survival probability of about 50%. The multimodal therapeutic scheme of NB includes isotretinoin (13cRA), used in the post-consolidation phase as an anti-proliferative and pro-differentiative agent to minimize residual disease and prevent relapse. Through a small molecule screening, we identified isorhamnetin (ISR) as a synergistic compound with 13cRA in inhibiting up to 80% of NB cell viability. To unveil the molecular mechanisms underlying this synergism, microarray analysis was performed in CHP134 control cells, and cells treated with 13cRA (5uM), ISR (15uM), and their combination. This analysis revealed that 13cRA ISR synergism is accompanied by a marked increase in the expression of the adrenergic receptor α1B (ADRA1B) gene. Administration of doxazosin, a safe α1-antagonist used in pediatric patients, with 13cRA in NB xenografted mice exerted a marked control of tumor growth, while each of the two drugs alone was ineffective. We, therefore, preclinically identify the α1B adrenergic receptor as a novel pharmacological target in NB. We propose evaluating the addition of α1-antagonists in the post-consolidation therapy of NB to more efficiently control residual disease. Keywords: isotretinoin, 13cRA, 13-cis retinoic acid, isorhamnetin, ISR, neuroblastoma, polysome profiling, translatome, adrenergic receptors, α-blockers, combinatorial therapy, synergy

2023-05-29 | GSE232388 | GEO

Genome-wide gene expression of NB-1 after treatment of 5-aza-dC, TBT, and combination

Project description:A neuroblastoma cell line, NB-1, was treated with mock, a DNA demethylating agent (5-aza-2'-deoxycytidine: 5-aza-dC), a synthetic retinoic acid (tamibarotene: TBT), and the combination of 5-aza-dC and TBT. A genome-wide gene expression analysis was performed using SurePrint G3 Human Gene Expression 8 x 60K v2 Microarray.

2021-07-23 | GSE180645 | GEO

Transcription profiling of human BE(2)-C neuronal responses to type I IFN stimulation

Project description:Human neuronal differentiation alters responsiveness to innate immune stimuli and virus infections. We used microarrays to examine the transcriptional responses of the human BE(2)-C neuroblastoma cell line to retinoic acid-induced differentiation and type I IFN stimulation. Experiment Overall Design: Cultured BE(2)-C cells were differentiated with 10 uM all-trans retinoic acid (RA) for 3 weeks, incubated with universal type I IFN (IFNa-A/D) for 6 or 12 h, and Affymetrix Human Genome Array U133 Plus 2.0 chips were used to analyze transcript levels.

2009-07-12 | E-GEOD-16450 | biostudies-arrayexpress

Super-enhancer-associated core regulatory circuits mediate susceptibility to retinoic acid in neuroblastoma cells [RNA-seq]

Project description:Neuroblastoma is a pediatric tumor that accounts for more than 15% of cancer-related deaths in children. Survival chances for high-risk patients are less than 50%. Retinoic acid treatment is part of the maintenance therapy given to neuroblastoma patients; however, not all tumors respond to retinoic acid-mediated differentiation. Among neuroblastoma tumors, two phenotypically distinct cell types-adrenergic (ADRN) and mesenchymal (MES), have been identified based on their super-enhancer landscape and transcriptional core regulatory circuitries. We hypothesized that distinct super-enhancers in these different tumor cells could mediate differential response to retinoic acid. To this end, we treated four different neuroblastoma cell lines, comprising both ADRN (MYCN amplified and non-amplified) and MES subtypes, with retinoic acid and studied the super-enhancer landscape upon treatment and after removal of retinoic acid. Using H3K27ac ChIP-seq paired with RNA-seq, we compared the super-enhancers in cells that respond to retinoic acid-mediated differentiation versus those that fail to differentiate. We identified unique super-enhancers associated with cells differentiation; however, even among cells that respond to treatment, there was heterogeneity upon removal of retinoic acid, with MYCN amplified cells remaining differentiated whereas MYCN non-amplified cells reverted to a proliferative state. This study identifies regulatory super-enhancers as a plausible mechanism behind the differential response to retinoic acid-mediated differentiation.

2022-07-28 | GSE201179 | GEO

Super-enhancer-associated core regulatory circuits mediate susceptibility to retinoic acid in neuroblastoma cells [ChIP-Seq]

2022-07-28 | GSE202239 | GEO

RNA-Seq of SH-SY5Y cells after DLG2 overexpression

Project description:The aim of this experiment is to study the gene expression response of DLG2 overexpression in neuroblastoma. Four different conditions were compared in neuroblastoma SH-SY5Y cells, with 4 biological replicates each: 1) Control (no DLG2 overexpression, no retinoic acid treatment), 2) RA (no DLG2 overexpression, retinoic acid treatment), 3) DLG2 (DLG2 overexpression, no retinoic acid treatment), 4) DLG2-RA (DLG2 overexpression, retinoic acid treatment)

2020-08-13 | E-MTAB-8657 | biostudies-arrayexpress

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