Expression data of progesterone regulated miRNAs in U251 cells, derived from human glioblastoma
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PROVIDER: PRJNA603058 | ENA |
REPOSITORIES: ENA
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Project description:Glioblastoma multiforme (GBM), a grade IV astrocytoma, is the most common and aggressive brain tumor in adults, characterized by being highly infiltrative, angiogenic, and resistant to chemotherapy and radiotherapy. In previous works, has been determined that progesterone P4 increases proliferation, migration and invasion of cells derived from human GBMs through the interaction with its intracellular receptor (PR). In breast cancer, there exist evidence that P4 regulates the expression of miRNAs with tumor suppressor or oncogenic action, via the classical PR. The signature of miRNAs affected by P4 treatment in cells derived from human GBMs has not been determined. Therefore, we studied the effect of P4 on miRNAs expression pattern in U251 cells derived from a human GBM.
2020-01-25 | GSE144204 | GEO
Project description:Missense point mutations in the TP53 gene are frequent genetic alterations in human tumor tissue and cell lines derived thereof. Mutant p53 (mutp53) proteins have lost sequence-specific DNA binding, but have retained the ability to interact in a structure-selective manner with non-B DNA and to act as regulators of transcription. To identify functional binding sites of mutp53, we established a small library of genomic sequences bound by p53R273H in U251 human glioblastoma cells using chromatin immunoprecipitation (ChIP). Mutp53 binding to isolated DNA fragments confirmed the specificity of the ChIP. The mutp53 bound DNA sequences are rich in repetitive DNA elements, which are dispersed over non-coding DNA regions. Stable down-regulation of mutp53 expression strongly suggested that mutp53 binding to genomic DNA is functional. We identified the PPARGC1A and FRMD5 genes as p53R273H targets regulated by binding to intronic and intra-genic sequences. We propose a model that attributes the oncogenic functions of mutp53 to its ability to interact with intronic and intergenic non-B DNA sequences and modulate gene transcription via re-organization of chromatin. For the study of the consequences of mutant p53 (R273H) knockdown on gene expression, total RNA from parental U251 glioblastoma cells and UsiA12 clone was prepared from two independent cell culture experiments (biological replicates) and processed for microarray-based profiling of gene expression. UsiA12 clone was derived from the U251 cells transfected with the pSuper-p53 and pCI-neo vectors.
2010-06-24 | E-GEOD-13991 | biostudies-arrayexpress
Project description:we report that U251 glioblastoma tumor spheres exhibit low cytosolic folate cycle and a reprogrammmed mitochondrial folate cycle that is presumably oriented towards oxidizing the formyl group to CO2 with the production of TetraHydroFolate and release of NADPH instead of synthesizing formate
2019-07-01 | GSE117543 | GEO
Project description:We examined the global gene expression pattern of T cells regulated by progesterone to gain further insights into the regulatory mechanisms of progesterone. We found 325-347 cord blood T cell genes up or down-regulated by P4 in the presence or absence of exogenous TGFb1. Peripheral blood T cells were relatively unresponsive with only 30-70 genes regulated by P4. IL-6 receptor (IL-6R) expression was greatly down-regulated by progesterone in cord blood, but not PB, T cells. Overall, these differences in gene expression are consistent with the differential responses of cord blood and peripheral blood T cells to progesterone. To gain insights into the differences of progesterone and control dendritic cells, we performed a microarray study and found ~180 genes regulated by progesterone in dendritic cells. The gene expression information suggests that progesterone has the potential to alter dendritic cell responses to cytokines, chemokine production, and migration which in combination would control T cell differentiation.
2012-03-02 | GSE22025 | GEO
Project description:BRD4 is a member of the bromodomain and extra-terminal (BET) family, which has become a promising drug target for numerous cancers. It has been reported that BRD4 is deregulated in gliomas; however, the precise molecular pathways regulated by BRD4 are still elusive. In this study, we knocked down BRD4 expression in glioma cell line U251 by lentivirus-mediated short hairpin RNA (shRNA) approach. BRD4 downregulation attenuated cell proliferation and promoted cell apoptosis. Genome-wide analysis of BRD4-regulated transcripts in U251 cells was performed using microarray to reveal the possible molecular mechanism
2017-04-15 | GSE97791 | GEO
Project description:We showed that DBTRG is more invasive than U251 cell lines by novel brain-stiffness-mimicking matrix gel invasion platform and transwell invasion assay. To understand the molecular mechanisms of DBTRG being more invasive than U251, we performed transcriptomic sequencing analysis of DBTRG and U251 cell lines.
2022-04-18 | GSE200574 | GEO
Project description:Glioblastomas (GBMs) are the most frequent and malignant type of brain tumor. It has been reported that progesterone (P4) regulates the progression of GBMs by modifying the expression of genes that promote cell proliferation, migration and invasion; however, it is not fully understood how these processes are regulated. It is possible that P4 mediates some of these effects through changes in the microRNA (miRNA) expression profile in GBM cells. The present study investigated the effects of P4 on miRNAs expression profile in U‑251MG cells derived from a human GBM. U‑251MG cells were treated for 6 h with P4, RU486 (an antagonist of the intracellular progesterone receptor), the combined treatment (P4+RU486) and cyclodextrin (vehicle) and then a miRNA microarray analysis conducted. The expression analysis revealed a set of 190 miRNAs with differential expression in the treatments of P4, RU486 and P4+RU486 in respect to the vehicle and P4 in respect to P4+RU486, of which only 16 were exclusively regulated by P4. The possible mRNA targets of the miRNAs regulated by P4 could participate in the regulation of proliferation, cell cycle progression and cell migration of GBMs. The present study provided insight for understanding epigenetic modifications regulated by sex hormones involved in GBM progression, and for identifying potential therapeutic strategies for these brain tumors.
| S-EPMC8097752 | biostudies-literature
Project description:Using human U251 glioblastoma cells with endogenous mutp53 expression as a model, we performed a ChIP-chip analysis of mutp53 binding sites on a custom tiling array, coupled with global expression profiling and an analysis of the epigenetic status of mutp53 regulated promoters. Mutp53 binds preferentially, and independent of other transcription factors (e.g. ETS1 and SP1), to G/C-rich DNA stretches around transcriptional start sites (TSS) of many genes. Mutp53-bound regions are frequently located in CpG islands and are highly prone to adopt non-B DNA conformation(s). Analysis of the transcriptional status of mutp53-regulated genes demonstrated that mutp53 generally modulates transcription from active promoters marked by H3K4me3. Based on our data we propose a dual mode model of mutp53 GOF, which includes both stochastic and deterministic components. On a local scale, mutp53 acts as a basal transcriptional co-factor that has the potential to bind autonomously and selectively to non-B DNA structures around TSSs of active genes and to modulate transcription rates of many genes in a context and stimulus-dependent fashion. Resulting stochastic alterations generate transcriptional plasticity and enhance transcriptional competence on a global scale. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2012-12-10 | E-GEOD-35500 | biostudies-arrayexpress
Project description:We examined the global gene expression pattern of T cells regulated by progesterone to gain further insights into the regulatory mechanisms of progesterone. We found 325-347 cord blood T cell genes up or down-regulated by P4 in the presence or absence of exogenous TGFb1. Peripheral blood T cells were relatively unresponsive with only 30-70 genes regulated by P4. IL-6 receptor (IL-6R) expression was greatly down-regulated by progesterone in cord blood, but not PB, T cells. Overall, these differences in gene expression are consistent with the differential responses of cord blood and peripheral blood T cells to progesterone. To gain insights into the differences of progesterone and control dendritic cells, we performed a microarray study and found ~180 genes regulated by progesterone in dendritic cells. The gene expression information suggests that progesterone has the potential to alter dendritic cell responses to cytokines, chemokine production, and migration which in combination would control T cell differentiation. The CD4+ CD25- T cells were isolated from cord blood and peripheral blood and cultured in the presence and absence of progesterone 2 ug per mL, TGFb1 150 pg/mL and IL-2 100u/mL for 5-6 days. T cells from cord blood and peripheral blood were compared.
2012-03-02 | E-GEOD-22025 | biostudies-arrayexpress