A set of changes is identified in the transcription profile associated with the long-term, but not the acute, response to radiation exposure. The study was performed in vivo using zebrafish.
Long-term effects of ionizing radiation on gene expression in a zebrafish model.
Age, Specimen part, Treatment
View SamplesThe ZMYM2-FGFR1 (formerly known as ZNF198-FGFR1) fusion kinase induces stem cell leukemia-lymphoma syndrome (SCLL), a hematological malignancy characterized by rapid transformation to acute myeloid leukemia and T-lymphoblastic lymphoma.
Constitutive Notch pathway activation in murine ZMYM2-FGFR1-induced T-cell lymphomas associated with atypical myeloproliferative disease.
Specimen part, Disease, Disease stage, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
HOXC9 directly regulates distinct sets of genes to coordinate diverse cellular processes during neuronal differentiation.
Specimen part, Cell line
View SamplesMetastatic human colon carcinoma cell lines LS411N and SW620 were cultured in the presence of increased concentration of 5-FU. The selected stable cell lines (LS411N-5FU-R and SW620-5FU-R) are CD133+ that are resistant to 5-FU. However, FACS-sorted CD133+ cells from LS411N and SW620 are not resistant to 5-FU, suggesting that only a subset of CD133+ cells are 5-FU-resistant colon cancer stem cells. A global gene expression profiling was performed to identify differentiated expressed genes between LS411N-CD133+ cells and LS411N-5FU-R, and between SW620-CD133+ and SW620-5FU-R cells. These differentially expressed genes are potentially responsible for the colon cancer stem cell phenotypes and chemoresistance.
No associated publication
Cell line
View SamplesWe performed microarray gene expression profiling to identify genes essential for the growth and tumorigenicity of mouse neuroblastoma stem-like cells
No associated publication
Specimen part
View SamplesThe microarray gene expression profiling reveals that the histone H3 demethylase KDM4C transcriptionally activates the serine-glycine pathway, stress responses and genes in control of cell-cycle progression.
No associated publication
Cell line, Treatment
View SamplesCell differentiation is an essential process of normal development by which a stem cell or progenitor cell becomes a post-mitotic, specialized cell with unique morphology and function. Also, it has long been recognized that differentiation is associated with a marked reduction in DNA damage response at the global level. The molecular basis for the coordination between cell cycle exit, acquirement of specialized structure and function, and attenuation of DNA damage response during differentiation is not well understood. We have conducted a genome-wide analysis of the HOXC9-induced neuronal differentiation program in human neuroblastoma cells. Gene expression profiling reveals that HOXC9-induced differentiation is associated with transcriptional regulation of 2,395 genes, which is characterized by global upregulation of neuronal genes and downregulation of cell cycle and DNA repair genes. Remarkably, genome-wide mapping demonstrates that HOXC9 occupies 40% of these genes, including a large number of genes involved in neuronal differentiation, cell cycle progression and DNA damage response. These findings suggest that HOXC9 directly activates and represses the transcription of distinct sets of genes to coordinate the cellular events characteristic of neuronal differentiation.
HOXC9 directly regulates distinct sets of genes to coordinate diverse cellular processes during neuronal differentiation.
Cell line
View SamplesIncreased activation of the serine-glycine biosynthetic pathway is an integral part of cancer metabolism that drives macromolecule synthesis needed for cell proliferation. Whether this pathway is under epigenetic control is unknown. Here we show that the histone H3 lysine 9 (H3K9) methyltransferase G9A is required for maintaining the pathway enzyme genes in an active state marked by H3K9 monomethylation and for the transcriptional activation of this pathway in response to serine deprivation. G9A inactivation depletes serine and its downstream metabolites, triggering cell death with autophagy in cancer cell lines of different tissue origins. Higher G9A expression, which is observed in various cancers and is associated with greater mortality in cancer patients, increases serine production and enhances the proliferation and tumorigenicity of cancer cells. These findings identify a G9A-dependent epigenetic program in the control of cancer metabolism, providing a rationale for G9A inhibition as a therapeutic strategy for cancer.
The histone H3 methyltransferase G9A epigenetically activates the serine-glycine synthesis pathway to sustain cancer cell survival and proliferation.
Treatment
View SamplesMEIS2 has an important role in development and organogenesis, and is implicated in the pathogenesis of human cancer. The molecular basis of MEIS2 action in tumorigenesis is not clear. Here, we show that MEIS2 is highly expressed in human neuroblastoma cell lines and is required for neuroblastoma cell survival and proliferation. Depletion of MEIS2 in neuroblastoma cells leads to M phase arrest and mitotic catastrophe, whereas ectopic expression of MEIS2 markedly enhances neuroblastoma cell proliferation, anchorage-independent growth, and tumorigenicity. Gene expression profiling reveals an essential role of MEIS2 in maintaining the expression of a large number of late cell cycle genes, including those required for DNA replication, G2-M checkpoint control and M phase progression. Importantly, we identify MEIS2 as a transcription activator of the MuvB-BMYB-FOXM1 complex that functions as a master regulator of mitotic gene expression. Further, we show that FOXM1 is a direct target gene of MEIS2 and is required for MEIS2 to upregulate mitotic genes. These findings link a development gene to the control of cell cycle progression and suggest that high MEIS2 expression is a molecular mechanism for high expression of mitotic genes that is commonly observed in cancers of poor prognosis.
MEIS2 is essential for neuroblastoma cell survival and proliferation by transcriptional control of M-phase progression.
Cell line, Treatment
View SamplesThe hypercellularity in the outer layers of the cortex in Lgi1 null mice suggested that Lgi1 possibly plays a role in controlling cell migration dynamics. To investigate this hypothesis, we first generated and immortalized neural precursor-like cells (NPC), isolated from Lgi1 null and wild type mice at E13.5 stage using Large-T antigen. Subsequently, we compared gene expression patterns between the immortalized NPC-like cells with the two different Lgi1 genotypes using Affymetrix GeneChip Mouse Gene 1.0 ST Array.
No associated publication
Specimen part
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