The sialic glycoprotein, Mucin1, is known to be involved in the pathogenesis of various types of cancers. In a fraction of patients with multiple myeloma, their myeloma cells have high Mucin1 expression. We established a myeloma cell line designated EMM1 from a myeloma patient whose myeloma cells have high Mucin1 expression. Then we performed knockdown of Mucin1 to elucidate the role of the high Mucin1 expression. Overall design: we performed knockdown of Mucin1 to elucidate the role of the high Mucin1 expression. Knockdown of MUC1 in EMM1 cells induced cell cycle arrest during S phase and apoptosis in EMM1 cells. To elucidate the role of Mucin1 in EMM1 cells, we generated EMM1 cells lines expressing shMucin1 or control shRNA and performed RNA-seq analysis of the two cell lines and compared the differences in gene expressions.
MUC1/KL-6 expression confers an aggressive phenotype upon myeloma cells.
Specimen part, Cell line, Subject
View SamplesThis study aimed to define the genes associated with PCNSL patient survival. Expression profiling was performed on 34 PCNSLs. A gene classifier was developed.
Gene expression signature-based prognostic risk score in patients with primary central nervous system lymphoma.
Sex, Age, Specimen part, Disease, Disease stage
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PU.1 is a potent tumor suppressor in classical Hodgkin lymphoma cells.
Cell line, Time
View SamplesPU.1 is an Ets family transcription factor that is essential for the differentiation of both myeloid and lymphoid cells. PU.1 is down-regulated in classical Hodgkin lymphoma cells via methylation of the PU.1 promoter. To evaluate whether down-regulation of PU.1 is essential for the growth of cHL cells, we generated KM-H2 derived cell lines conditionally express PU.1 by tet-off system (designated KM-H2tetPU.1). Conditonally expressed PU.1 by tetracycline removal induced complete growth arrest and apoptosis in KM-H2 cells. To elucidate the mechanisms underlying cell cycle arrest and apoptosis induced by PU.1, we compared gene expression profiles of KM-H2tetPU.1 cells 0, 1 and 3 days after PU.1 induction, by DNA microarray.
PU.1 is a potent tumor suppressor in classical Hodgkin lymphoma cells.
Cell line, Time
View SamplesGlioma initiating cells (GICs) are considered responsible for the therapeutic resistance and recurrence of malignant glioma. To clarify the molecular mechanism of GIC maintenance/differentiation, we established GIC clones from GBM patient tumors having the potential to differentiate into malignant gliomas in mouse intracranial xenograft, and established an in vitro glioma induction system by using serum stimulation.
Glioma initiating cells form a differentiation niche via the induction of extracellular matrices and integrin αV.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Defining CD4 T cell memory by the epigenetic landscape of CpG DNA methylation.
No sample metadata fields
View SamplesMemory T cells are primed for rapid responses to antigen; however, the molecular mechanisms responsible for priming remain incompletely defined. CpG methylation in promoters is an epigenetic modification, which regulates gene transcription. Using targeted bisulfite sequencing, we examined methylation of 2100 genes (56,000 CpG) mapped by deep sequencing to T cell activation in human nave and memory CD4 T cells. 466 CpGs (132 genes) displayed differential methylation between nave and memory cells. 21 genes exhibited both differential methylation and gene expression before activation, linking promoter DNA methylation states to gene regulation; 6 genes encode proteins closely studied in T cells while 15 genes represent novel targets for further study. 39 genes exhibited reduced methylation in memory cells coupled with increased gene expression with activation compared to nave cells, revealing specific genes more rapidly expressed in memory compared to nave cells and potentially regulated by DNA methylation. These findings define a DNA methylation signature unique to memory CD4 T cells and correlated with activation-induced gene expression.
Defining CD4 T cell memory by the epigenetic landscape of CpG DNA methylation.
No sample metadata fields
View SamplesMemory T cells are primed for rapid responses to antigen; however, the molecular mechanisms responsible for priming remain incompletely defined. CpG methylation in promoters is an epigenetic modification, which regulates gene transcription. Using targeted bisulfite sequencing, we examined methylation of 2100 genes (56,000 CpG) mapped by deep sequencing to T cell activation in human naïve and memory CD4 T cells. 466 CpGs (132 genes) displayed differential methylation between naïve and memory cells. 21 genes exhibited both differential methylation and gene expression before activation, linking promoter DNA methylation states to gene regulation; 6 genes encode proteins closely studied in T cells while 15 genes represent novel targets for further study. 39 genes exhibited reduced methylation in memory cells coupled with increased gene expression with activation compared to naïve cells, revealing specific genes more rapidly expressed in memory compared to naïve cells and potentially regulated by DNA methylation. These findings define a DNA methylation signature unique to memory CD4 T cells and correlated with activation-induced gene expression. Overall design: RNA sequencing of primary human naïve and memory CD4 T cells at rest and 48 hours post-activation.
Defining CD4 T cell memory by the epigenetic landscape of CpG DNA methylation.
No sample metadata fields
View SamplesCombinatorial control of gene expression by the three yeast repressors Mig1, Mig2 and Mig3
Combinatorial control of gene expression by the three yeast repressors Mig1, Mig2 and Mig3.
No sample metadata fields
View Samples10 + 10 Holstein x Charolais F2 cattle were assigned to 2 groups with high and low IMF content, respectively; Musculus longissimus dorsi mRNA expression was determined by microarray analysis
Gene expression profile of Musculus longissimus dorsi in bulls of a Charolais × Holstein F2-cross with divergent intramuscular fat content.
Specimen part
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