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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Ivan Arisi

PROVIDER: E-GEOD-30677 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Lamin A/C Is Required For ChAT-Dependent Neuroblastoma Differentiation: a microarray gene expression study

Project description:The mouse neuroblastoma N18TG2 clone is unable to differentiate and defective for the enzymes of the biosynthesis of neurotransmitters. The forced expression of choline acetyltransferase (ChAT) in these cells results in the synthesis and release of acetylcholine (Ach) and hence in the expression of neurospecific features and markers. To understand how the expression of ChAT triggered neuronal differentiation, we studied the differences in genome-wide transcription profiles between the N18TG2 parental cells and its ChAT-expressing 2/4 derived clone. The engagement of the 2/4 cells in the neuronal developmental programme was confirmed by the increase of the expression level of several differentiation-related genes and by the reduction of the amount of transcripts of cell-cycle genes. At the same time, we observed a massive reorganisation of cytoskeletal proteins in terms of gene expression, with the accumulation of the nucleoskeletal lamina component Lamin A/C in differentiating cells. The increase of the Lmna transcripts induced by ChAT-espression in 2/4 cells was mimicked treating the parental N18TG2 cells with the acetylcholine-receptor agonist carbachol, thus demonstrating the direct role played by this receptor in neuron nuclei maturation. Conversely, a treatment of 2/4 cells with the muscarinic-receptor antagonist atropine resulted in the reduction of the amount of Lmna RNA. Finally, the hypothesis that Lmna gene product might play a crucial role in the ChAT-dependent molecular differentiation cascade was strongly supported by Lmna knock-down in 2/4 cells leading to the down-regulation of genes involved in differentiation and cytoskeleton formation and to the up-regulation of genes known to regulate self-renewal and stemness. The gene expression profile of the ChAT-expressing 2/4 clone was compared to that of the N18TG2 parental cells, with and without retinoic acid (RA) stimulation using Agilent microarray analysis.

2017-04-18 | E-GEOD-73591 | biostudies-arrayexpress

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.

2013-07-11 | GSE30677 | GEO

Spatially restricted position-dependent implications of lamin A promoter occupancy on gene activity (expression)

Project description:Interactions between the nuclear lamina (NL) and chromatin are thought to occur through large lamin association domains (LADs) and correlate with gene repression in these domains. We show that binding of lamin A/C (LMNA) to promoters occurs on discrete domains that are associated with distinct transcriptional outputs. Chromatin immunoprecipitation identifies thousands of LMNA-bound promoters, primarily linked to signaling functions. LMNA often occupies narrow domains on promoters, yet LMNA-bound promoters are often contiguous. LMNA-bound genes are overall repressed, but repression correlates with co-enrichment in repressive histone marks rather than LMNA occupancy per se. Genes marked by LMNA and H3K4me3 escape LMNA-associated repression in the absence of repressive histone marks. Positioning of LMNA on promoters relative to the TSS correlates with distinct transcriptional outputs: whereas upstream-distal binding can be transcriptionally permissive, TSS occupancy is associated with promoter inactivity. Perturbation in NL organization causes reorganization of lamin promoter occupancy and uncouples LMNA binding from promoter inactivity. Our results show the existence of many spatially restricted LMNA binding events on promoter regions, with distinct position-dependent transcriptional outputs. Total RNA obtained from ASCs and ASCs depleted of LMNA (LMNA-KD) and processed for microarray hybridization.

2013-07-14 | E-GEOD-42523 | biostudies-arrayexpress

Neural induction (Embrioid bodies-Retinoic acid)

Project description:Neural induction of ES by Retinoic acid Neural induction of ES by Retinoic acid

2010-06-11 | E-GEOD-4075 | biostudies-arrayexpress

Retinoids induce rapid dynamic changes in the non-coding RNAs and epigenetic profiles of murine Hox clusters (tiling)

Project description:Physiologically relevant concentrations of retinoic acid are added to Mouse ES cells and a time course (0-72 hours) is examined with expression tiling arrays to characterize the early dynamics of expression of coding and non-coding RNAs in and around the Hox clusters. Gene expression is examined at various timepoints (0-72 hrs) after retinoic acid induced neuronal differentiation

2015-04-27 | E-GEOD-61585 | biostudies-arrayexpress

Spatially restricted position-dependent implications of lamin A promoter occupancy on gene activity (ChIPs and MeDips)

Project description:Interactions between the nuclear lamina (NL) and chromatin are thought to occur through large lamin association domains (LADs) and correlate with gene repression in these domains. We show that binding of lamin A/C (LMNA) to promoters occurs on discrete domains that are associated with distinct transcriptional outputs. Chromatin immunoprecipitation identifies thousands of LMNA-bound promoters, primarily linked to signaling functions. LMNA often occupies narrow domains on promoters, yet LMNA-bound promoters are often contiguous. LMNA-bound genes are overall repressed, but repression correlates with co-enrichment in repressive histone marks rather than LMNA occupancy per se. Genes marked by LMNA and H3K4me3 escape LMNA-associated repression in the absence of repressive histone marks. Positioning of LMNA on promoters relative to the TSS correlates with distinct transcriptional outputs: whereas upstream-distal binding can be transcriptionally permissive, TSS occupancy is associated with promoter inactivity. Perturbation in NL organization causes reorganization of lamin promoter occupancy and uncouples LMNA binding from promoter inactivity. Our results show the existence of many spatially restricted LMNA binding events on promoter regions, with distinct position-dependent transcriptional outputs. ChIPs were done from cultured untreated and LMNA-downregulated adipose stem cell (ASC) chromatin. MeDIPs were done from LMNA-downregulated ASCs. ChIP and MeDIP DNA was hybridized onto the aforementioned HG-18 Nimbegen promoter arrays.

2013-07-14 | E-GEOD-42522 | biostudies-arrayexpress

Transcription profiling of mouse ES cell embrioid bodies treated with retinoic acid

Project description:Neural induction of ES by Retinoic acid

2005-01-01 | E-MNIA-63 | biostudies-arrayexpress

Stage-dependent gene expression change in Sertoli cells regulated by retinoic acid signaling

Project description:To identifiy stage-dependent genes in Sertoli cells, we performed expression microarray analysis of the adult whole testes, cultured primary Sertoli cells, Sertoli cells directly isolated from wild-type and Nanos3 (germ-less) testes,seminiferous tubules at stages I-III, IV-VI, VII-VIII and IX-XII. Next to examine the relationship between stage-dependent gene expression change and retinoic acid signaling, we performed expression microarray analysis of the cultured primary Sertoli cells treated with retinoic acid and stage-specific seminiferous tubules injected with lentivirus containing Venus or dominat negative form of RARa, a dominant receptor for retinoic acid in Sertoli cells. Biological duplicates were examined at each sample

2012-06-30 | E-GEOD-34758 | biostudies-arrayexpress

Transcription profiling of primary fibroblasts from a family with autosomal recessive Hutchinson-Gilford Progeria Syndrome

Project description:Hutchinson-Gilford progeria syndrome (HGPS) is a genetic disorder displaying features reminiscent of premature senescence caused by germline mutations in the LMNA gene encoding lamin A and C, essential components of the nuclear lamina. By studying a family with homozygous LMNA mutation (K542N), we showed that HGPS can also be caused by mutations affecting both isoforms, lamin A and C (J Med Genet 2004;41:609M-^V614). With the aim to elucidate the molecular mechanisms underlying the pathogenesis of lamin A/C-related (hereditary) HGPS, we investigated primary cultured skin fibroblasts from affected homozygous K542N carriers (n=3), healthy heterozygotes (n=3), and controls (n=3) for differences in global gene expression using GeneChip Human Genome U133 Plus 2.0 arrays (Affymetrix UK Ltd.).

2011-06-27 | E-MEXP-3097 | biostudies-arrayexpress

Retinoic acid and Azakenpoullone treatment in SH-SY5Y/6TR(EU)/pTrex-Dest-30/MYCN cell line in high and low MYCN levels

Project description:The effect of the GSK3 inhibitor Azakenpaullone (Azak) and the differentiation agent retinoic acid (RA) was studied in low and high MYCN levels in the MYCN inducible neuroblastoma cell line SH-SY5Y/6TR(EU)/pTrex-Dest-30/MYCN (SY5Y-MYCN). Azak was dissolved in DMSO in order to apply it to the cells. Therefore a vehicle control consisting of SY5Y-MYCN cells treated with 24h 1 ul/ml DMSO only was used in duplicates. Doxycycline (Sigma) dissolved in water was used at a final concentration of 1ug/ml to induce MYCN expression in SY5Y-MYCN. A co-treatment study with Dox and Azak was conducted. SY5Y-MYCN cells were treated with 24h Azak, 24h Azak & 48h Dox and 48h Dox, with biological duplicates. 1 uM RA (dissolved in DMSO) and 1 ug/mL Doxycycline were given individually and in combination. SY5Y-MYCN cells were treated with 24h RA, 24h RA & 48h Dox, and 48h Dox and RNA was extracted in biological duplicates. For the 24h RA & 48h Dox co-treatment cells were treated with Dox for 24h and then with RA and fresh Dox for a further 24h.

2015-06-30 | E-MTAB-2689 | biostudies-arrayexpress

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