DAOY human medulloblastoma cells stably expressing a tamoxifen inducible MXD3: Ethanol vs. Tamoxifen
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE58903 | GEO | 2014/06/28
SECONDARY ACCESSION(S): PRJNA253842
REPOSITORIES: GEO
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE34050: ChIP-chip from DAOY cells stably expressing HA-MXD3 with anti-HA GSE34100: Expression profiling of MXD3 stable cell lines Refer to individual Series
2012-07-12 | E-GEOD-34101 | biostudies-arrayexpress
Project description:A subset of medulloblastomas, the most common brain tumor in children, is hypothesized to originate from granule neuron precursors (GNPs) in which the sonic hedgehog (SHH) pathway is over-activated. MXD3, a basic helix-look-helix zipper transcription factor of the MAD family, has been reported to be upregulated during postnatal cerebellar development and to promote GNP proliferation and MYCN expression. Mxd3 is upregulated in mouse models of medulloblastoma as well as in human medulloblastomas. Therefore, we hypothesize that MXD3 plays a role in the cellular events that lead to medulloblastoma biogenesis. The purpose of this study was to identify MXD3 target genes.
2012-07-13 | GSE34050 | GEO
Project description:A subset of medulloblastomas, the most common brain tumor in children, is hypothesized to originate from granule neuron precursors (GNPs) in which the sonic hedgehog (SHH) pathway is over-activated. MXD3, a basic helix-look-helix zipper transcription factor of the MAD family, has been reported to be upregulated during postnatal cerebellar development and to promote GNP proliferation and MYCN expression. Mxd3 is upregulated in mouse models of medulloblastoma as well as in human medulloblastomas. Therefore, we hypothesize that MXD3 plays a role in the cellular events that lead to medulloblastoma biogenesis. The purpose of this study was to identify MXD3 target genes. Stable cell line overexpressing HA tagged MXD3 immunoprecipitated with anti-HA; 2 biological replicates on 2 promoter arrays
2012-07-12 | E-GEOD-34050 | biostudies-arrayexpress
Project description:A subset of medulloblastomas, the most common brain tumor in children, is hypothesized to originate from granule neuron precursors (GNPs) in which the sonic hedgehog (SHH) pathway is over-activated. MXD3, a basic helix-look-helix zipper transcription factor of the MAD family, has been reported to be upregulated during postnatal cerebellar development and to promote GNP proliferation and MYCN expression. Mxd3 is upregulated in mouse models of medulloblastoma as well as in human medulloblastomas. Therefore, we hypothesize that MXD3 plays a role in the cellular events that lead to medulloblastoma biogenesis. The purpose of this study was to identify changes in gene expression in response to MXD3. RNA from MXD3 stable cell lines compared to vector-only cell lines and to parental (DAOY) cell line.
2012-07-12 | E-GEOD-34100 | biostudies-arrayexpress
Project description: Not available
| S-EPMC3393725 | biostudies-literature
Project description:The goal of this study was to profile the total proteome and transcriptome of the established medulloblastoma cell lines, Daoy and UW228, using label-free nano-LC-MS/MS-based quantitative proteomics and high-throughput RNA sequencing (RNA-Seq), coupled with pathway analysis to identify differentially expressed genes, proteins and signaling pathways with potential as prognostic markers. A total of 14250 and 12870 transcripts were detected for Daoy and UW228, respectively. Proteomic profiling identified 2630 and 1235 proteins in Daoy and UW228, representing 18% and 10% of detected transcripts, respectively. Interestingly, Daoy proteome included >50% unique proteins, while almost 90% of proteins expressed by UW228 were commonly expressed in Daoy. Differential expression of a number of adhesion, cytoskeletal and signaling molecules were observed between the two cell lines. Upregulation of a number of proteins and enrichment of key signaling pathways, including WNT, Sonic hedgehog (SHH) and integrin signaling pathways, were uniquely observed in MB cell lines, in particular in Daoy.
2017-10-27 | PXD002659 | Pride
Project description:A subset of medulloblastomas, the most common brain tumor in children, is hypothesized to originate from granule neuron precursors (GNPs) in which the sonic hedgehog (SHH) pathway is over-activated. MXD3, a basic helix-look-helix zipper transcription factor of the MAD family, has been reported to be upregulated during postnatal cerebellar development and to promote GNP proliferation and MYCN expression. Mxd3 is upregulated in mouse models of medulloblastoma as well as in human medulloblastomas. Therefore, we hypothesize that MXD3 plays a role in the cellular events that lead to medulloblastoma biogenesis. The purpose of this study was to identify changes in gene expression in response to MXD3.
2012-07-13 | GSE34100 | GEO
Project description:To investigate the functional significance of STIM1::MXD3, we overexpressed the fusion gene in K562 myeloid leukemia cells and analysed global gene expression changes using RNA-seq.
2023-05-02 | GSE222813 | GEO
Project description: Not available
| S-EPMC4226952 | biostudies-literature
Project description:Aberrant activation of Hedgehog (HH) signaling has been identified as a key etiologic factor of many human malignancies. Signal strength, target gene specificity, and oncogenic activity of HH signaling profoundly depend on interactions with other pathways such as epidermal growth factor receptor-mediated signaling which has been shown to cooperate with HH/GLI in basal cell carcinoma and pancreatic cancer. We demonstrate that the human medulloblastoma cell line Daoy possesses a fully inducible endogenous HH pathway. Treatment of Daoy cells with Sonic Hedgehog or Smoothened agonist induced expression of GLI1 protein and prevented processing of GLI3 to its repressor form. To study interactions between HH- and EGF-induced signaling in greater detail, time-resolved measurements were carried out and analyzed on the transcriptomic as well as proteomic level. Daoy cells responded to the co-treatment by downregulating GLI1, PTCH, and HHIP on the transcript level which was also seen when Amphiregulin (AREG) was used instead of EGF. The finding that EGFR signaling silences proteins acting as negative regulators of HH signaling is firstly described here as a novel crosstalk mechanism. Furthermore, combined EGFR/HH signaling maintains high GLI1 protein levels contrasting its downregulation on the transcript level. On the other hand, high level synergism was observed with respect to a strong and significant upregulation of numerous canonical EGF-targets with putative tumor-promoting properties such as MMP7, VEGFA, and IL-8. In conclusion, synergistic effects between EGFR and HH signaling can selectively induce a switch from a canonical HH/GLI profile to a modulated specific target gene profile pointing to more wide-spread, yet context-dependent, interactions between HH/GLI and growth factor receptor signaling in human malignancies. To study interactions between HH- and EGF-induced signaling, time-resolved measurements were carried out over a period of 24 h at 14 different time points after stimulation by EGF with and without additional stimulation by SHH. Furthermore, as a control, cells without any stimulation by EGF and SHH (control) and cells in the presents of SHH were analyzed. Overall, three biological replicates of 60 different treatment/timepoints were analyzed yielding 180 different samples.
2014-07-31 | E-GEOD-46045 | biostudies-arrayexpress