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Sequential gene regulatory events leading to glucocorticoid-evoked apoptosis of CEM human leukemic cells

ABSTRACT: Sequential gene regulatory events leading to glucocorticoid-evoked apoptosis of CEM human leukemic cells

PROVIDER: PRJNA414180 | ENA |

REPOSITORIES: ENA

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Sequential gene regulatory events leading to glucocorticoid-evoked apoptosis of CEM human leukemic cells [HG_U95Av2]

Project description:Sequential gene regulatory events leading to glucocorticoid-evoked apoptosis of CEM human leukemic cells [HG_U95Av2]

| PRJNA414184 | ENA

Sequential gene regulatory events leading to glucocorticoid-evoked apoptosis of CEM human leukemic cells [HG-U133_Plus_2]

Project description:Sequential gene regulatory events leading to glucocorticoid-evoked apoptosis of CEM human leukemic cells [HG-U133_Plus_2]

| PRJNA414183 | ENA

Sequential gene regulatory events leading to glucocorticoid-evoked apoptosis of CEM human leukemic cells [HG_U95Av2]

Project description:Glucocorticoid (GC)- sensitive cells are killed by receptor (GR)-filling concentrations of GC for a sufficient time. We used 3 closely related clones (2 sensitive, 1 resistant) from the CEM line of ALL cells to test the hypothesis that over time, a distinct set of regulated genes would be found in sensitive clones, with cross-talk to other significant pathways

2017-10-14 | GSE104930 | GEO

Sequential gene regulatory events leading to glucocorticoid-evoked apoptosis of CEM human leukemic cells [HG-U133_Plus_2]

Project description:Glucocorticoid (GC)- sensitive cells are killed by receptor (GR)-filling concentrations of GC for a sufficient time. We used 2 closely related clones ( sensitive, 1 resistant) from the CEM line of ALL cells to test the hypothesis that at this early pre-apoptosis time, a distinct set of regulated genes would be found in the sensitive clones, with cross-talk to other significant pathways

2017-10-14 | GSE104931 | GEO

Sequential gene regulatory events leading to glucocorticoid-evoked apoptosis of CEM human leukemic cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-10-14 | GSE104932 | GEO

Sequential gene regulatory events leading to glucocorticoid-evoked apoptosis of CEM human leukemic cells:interactions of MAPK, MYC and glucocorticoid pathways.

Project description:Gene expression responses to glucocorticoid (GC) in the hours preceding onset of apoptosis were compared in three clones of human acute lymphoblastic leukemia CEM cells. Between 2 and 20h, all three clones showed increasing numbers of responding genes. Each clone had many unique responses, but the two responsive clones showed a group of responding genes in common, different from the resistant clone. MYC levels and the balance of activities between the three major groups of MAPKs are known important regulators of glucocorticoid-driven apoptosis in several lymphoid cell systems. Common to the two sensitive clones were changed transcript levels from genes that decrease amounts or activity of anti-apoptotic ERK/MAPK1 and JNK2/MAPK9, or of genes that increase activity of pro-apoptotic p38/MAPK14. Down-regulation of MYC and several MYC-regulated genes relevant to MAPKs also occurred in both sensitive clones. Transcriptomine comparisons revealed probable NOTCH-GC crosstalk in these cells.

| S-EPMC6075652 | biostudies-literature

E4BP4 facilitates glucocorticoid-evoked apoptosis of human leukemic CEM cells via upregulation of Bim.

Project description:BackgroundSynthetic GCs serve as therapeutic agents for some lymphoid leukemias because of their ability to induce transcriptional changes via the GC receptor (GR) and trigger apoptosis. Upregulation of the BH3-only member of Bcl-2 family proteins, Bim, has been shown to be essential for GC-evoked apoptosis of leukemic lymphoblasts. Using human T cell leukemic sister clones CEM-C7-14 and CEM-C1-15, we have previously shown that the bZIP transcriptional repressor, E4BP4, is preferentially upregulated by GCs in CEM-C7-14 cells that are susceptible to GC-evoked apoptosis, but not in refractory CEM-C1-15 cells. E4BP4 is an evolutionarily conserved member of the PAR family of bZIP transcription factors related to the C. elegans death specification gene ces2.ResultsMouse E4BP4 was ectopically expressed in CEM-C1-15 cells, resulting in sensitization to GC-evoked apoptosis in correlation with restoration of E4BP4 and Bim upregulation. shRNA mediated modest knockdown of E4BP4 in CEM-C7-14 cells resulted in concomitant reduction in Bim expression, although GC-evoked fold-induction and sensitivity to apoptosis was similar to parental cells.ConclusionData presented here suggest that GC-mediated upregulation of E4BP4 facilitates Bim upregulation and apoptosis of CEM cells. Since the Bim promoter does not contain any consensus GRE or EBPRE sequences, induction of Bim may be a secondary response.

| S-EPMC3197565 | biostudies-literature

Calcium-dependent upregulation of E4BP4 expression correlates with glucocorticoid-evoked apoptosis of human leukemic CEM cells.

Project description:Glucocorticoid (GC)-evoked apoptosis of T-lymphoid cells is preceded by increases in the intracellular Ca2+ concentration ([Ca2+]i), which may contribute to apoptosis. This report demonstrates that GC-mediated upregulation of the bZIP transcriptional repressor gene, E4BP4, is dependent on [Ca2+]i levels, and correlates with GC-evoked apoptosis of GC-sensitive CEM-C7-14 cells. Calcium chelators EGTA and BAPTA reduced [Ca2+]i levels and protected CEM-C7-14 cells from Dex-evoked E4BP4 upregulation as well as apoptosis. In the GC-resistant sister clone, CEM-C1-15, Dex treatment did not induce [Ca2+]i levels, E4BP4 expression or apoptosis, however, the calcium ionophore A23187 restored Dex-evoked E4BP4 upregulation and apoptosis. CEM-C7-14 cells were more sensitive to GC-independent increases in [Ca2+]i levels by thapsigargin, and a corresponding increase in E4BP4 expression and cell death, compared to CEM-C1-15 cells, suggesting a direct correlation between [Ca2+]i levels, E4BP4 expression, and apoptosis.

| S-EPMC2763529 | biostudies-literature

Human CEM Cells: Control vs. 2h or 4.5h Cluvenone Treated

Project description:Transcriptional profiling of human CEM cells comparing control untreated CEM cells with either 2h or 4.5h cluvenone-treated CEM cells.

2010-08-11 | GSE23536 | GEO

Human CEM Cells: Control vs. 2h or 4.5h Cluvenone Treated

Project description:Transcriptional profiling of human CEM cells comparing control untreated CEM cells with either 2h or 4.5h cluvenone-treated CEM cells. Two-timepoint experiment, CEM vs. Cluvenone-Treated CEM (2h and 4.5h). Biological replicates: 4 control, 4 2h-treated, 4 4.5h-treated, independently grown and harvested. Pooled controls. One replicate per array.

2010-08-11 | E-GEOD-23536 | biostudies-arrayexpress

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