E-GEOD-22139
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA127579
PROVIDER: E-GEOD-22139 | ExpressionAtlas | 2025-01-24
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-22139-analysis-methods.tsv | Tabular | |||
| E-GEOD-22139-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-22139-configuration.xml | Xml | |||
| E-GEOD-22139-percentile-ranks.tsv | Tabular | |||
| E-GEOD-22139.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 125 |
Shared Molecules
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Similar Datasets
Project description:Bone morphogenetic protein-7 is a MYC target with pro-survival functions in childhood medulloblastoma
| PRJNA127579 | ENA
Project description:Medulloblastoma (MB) is the most common malignant brain tumor in children, among whom overexpression or amplification of MYC oncogenes has been associated with poor clinical outcome. Although the MYC functions during normal development and oncogenesis in various systems have been extensively investigated, the transcriptional targets mediating MYC effects in MB are still elusive. Their identification and roles during MB onset and progression are important and will ultimately suggest novel potential therapeutic targets. cDNA microarray analysis was used to compare the effects of overexpressing and silencing MYC on the transcriptome of a MB-derived cell line. We identified 209 genes with potential relevance to MYC-dependent cellular responses in MB. Among the MYC-responsive genes, we found members of the bone morphogenetic protein (BMP) signaling pathway, which plays a crucial role during the development of the cerebellum. In particular, the cytokine gene BMP7 was identified as a direct target of MYC in MB cells. Similar to the effect induced by BMP7 silencing by siRNA, the use of a small-molecule inhibitor of the BMP/SMAD signaling pathway reduced cell viability in a panel of MB cells. Altogether, our findings indicate that high MYC levels drive BMP7 expression in MB to induce pro-survival and pro-proliferative cellular pathways. This observation suggests that targeting the BMP/SMAD pathway may be a new therapeutic concept for the treatment of childhood MB. 6 samples (3 replicates for each sample): wild-type MB cell line, empty vector-transfected control cell line, 2 c-MYC-overexpressing clones, 1 clone upon c-MYC silencing, 1 silencing control cell line.
2011-05-16 | E-GEOD-22139 | biostudies-arrayexpress
Project description:Medulloblastoma (MB) is the most common malignant brain tumor in children, among whom overexpression or amplification of MYC oncogenes has been associated with poor clinical outcome. Although the MYC functions during normal development and oncogenesis in various systems have been extensively investigated, the transcriptional targets mediating MYC effects in MB are still elusive. Their identification and roles during MB onset and progression are important and will ultimately suggest novel potential therapeutic targets. cDNA microarray analysis was used to compare the effects of overexpressing and silencing MYC on the transcriptome of a MB-derived cell line. We identified 209 genes with potential relevance to MYC-dependent cellular responses in MB. Among the MYC-responsive genes, we found members of the bone morphogenetic protein (BMP) signaling pathway, which plays a crucial role during the development of the cerebellum. In particular, the cytokine gene BMP7 was identified as a direct target of MYC in MB cells. Similar to the effect induced by BMP7 silencing by siRNA, the use of a small-molecule inhibitor of the BMP/SMAD signaling pathway reduced cell viability in a panel of MB cells. Altogether, our findings indicate that high MYC levels drive BMP7 expression in MB to induce pro-survival and pro-proliferative cellular pathways. This observation suggests that targeting the BMP/SMAD pathway may be a new therapeutic concept for the treatment of childhood MB.
2011-05-16 | GSE22139 | GEO
Project description:Epigenetic alterations contribute to leukemogenesis in childhood acute myeloid leukemia (AML). We used RNAi screens of AML cells together with non-transformed bone marrow cells and identified CHD4 as being required for AML maintenance. RNAi and CRISPR-Cas9 approaches, showed that CHD4 is essential for cell growth of leukemic cells in vitro, and disease progression in vivo, including primary childhood AML cells. Loss of function of CHD4 arrests AML cells in the G0 phase of the cell cycle, which is associated with downregulation of MYC and its target genes. Conversely, CHD4 suppression is not essential for normal blood cells. Taken together, our results identify CHD4 as a potential therapeutic target in childhood AML.
2018-11-01 | GSE106392 | GEO
Project description:Dysregulation of the proto-oncogene c-Myc (MYC henceforward) drives malignant progression, but also induces robust anabolic and proliferative programs leading to intrinsic stress. The mechanisms enabling adaptation to MYC-induced stress are not fully understood. We have uncovered an essential role for the transcription factor ATF4 in cell survival following MYC activation. MYC- upregulates ATF4 by activating GCN2 kinase through uncharged tRNAs. Subsequently, ATF4 co-occupies promoter regions of over 30 MYC target genes, including those regulating amino acid biosynthesis/transport and protein synthesis. ATF4 is essential for MYC-induced upregulation of the negative translational regulator and mTOR target 4E-BP1 and genetic or pharmacological inhibition of mTOR signaling rescues ATF4 deficient cells from MYC-induced stress. Acute deletion of ATF4 significantly delays MYC-driven tumor progression and increases survival in mouse models. Our results establish ATF4 as a cellular rheostat of MYC-activity, ensuring enhanced translation rates are compatible with survival and tumor progression.
2018-07-18 | GSE117240 | GEO
Project description:Neuroblastoma is an often intractable tumor that accounts for 15% of childhood cancer deaths. In addition to MYCN amplification in 20% of tumors, 11% express high levels of c-MYC (MYC) protein. To study this newly defined subgroup, we have created a novel transgenic zebrafish model in which overexpression of MYC in the peripheral sympathetic nervous system drives early-onset neuroblastoma.
2019-06-01 | GSE99566 | GEO
Project description:Rhabdomyosarcoma (RMS) is the most common soft-tissue sarcoma of childhood characterized by the inability to exit the proliferative myoblast-like stage. Here, we identified the DEAD box RNA helicase 5 (DDX5) as a potential therapeutic target to inhibit alveolar rhabdomyosarcoma (ARMS) growth. We show that DDX5 is overexpressed in alveolar RMS cells, demonstrating that its depletion drastically decreases ARMS viability and slows tumor growth in xenograft models. Mechanistically, we provide evidence that DDX5 functions upstream the G9a/AKT survival signalling pathway, by modulating G9a protein stability
2022-08-22 | GSE152358 | GEO
Project description:Rhabdomyosarcoma (RMS) is the most common soft-tissue sarcoma of childhood characterized by the inability to exit the proliferative myoblast-like stage. Here, we identified the DEAD box RNA helicase 5 (DDX5) as a potential therapeutic target to inhibit alveolar rhabdomyosarcoma (ARMS) growth. We show that DDX5 is overexpressed in alveolar RMS cells, demonstrating that its depletion drastically decreases ARMS viability and slows tumor growth in xenograft models. Mechanistically, we provide evidence that DDX5 functions upstream the G9a/AKT survival signalling pathway, by modulating G9a protein stability
2022-08-22 | GSE175455 | GEO
Project description:Gene Expression Classifiers for Minimal Residual Disease and Relapse Free Survival Improve Outcome Prediction and Risk Classification in Children with High Risk Acute Lymphoblastic Leukemia: A Children's Oncology Group Study willm-00140 Assay Type: Gene Expression Provider: Affymetrix Array Designs: HG-U133_Plus_2 Organism: Homo sapiens (ncbitax) Tissue Sites: Blood, Bone marrow Material Types: Peripheral Blood, Bone Marrow Disease States: Childhood Precursor B-Lymphoblastic Leukemia
2015-05-12 | E-GEOD-68735 | biostudies-arrayexpress
Project description:We previously described the use of a spotted oligonucleotide array to identify the mir-17 cluster as a direct transcriptional target of Myc. In order to determine whether Myc regulates additional miRNAs, we produced custom microarrays with an expanded set of probes capable of assaying the expression of 313 human miRNAs and 233 mouse miRNAs. miRNA expression was assayed in a murine model of Myc-induced B cell lymphoma. In this system, bone marrow from p53-/- mice is infected with a retrovirus that produces a Myc-estrogen receptor fusion protein (MycER). Infected cells form polyclonal B cell lymphomas in the presence of 4-hydroxytamoxifen (4-OHT), which activates the MycER fusion protein. RNA from subcutaneous tumors with high Myc activity (animals treated continuously with 4-OHT) and low Myc activity (animals in which 4-OHT was withdrawn after tumor formation) was analyzed. Keywords: Dose Response
2007-12-05 | GSE9104 | GEO