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GSE117611
Homo sapiens
12 Downloadable Samples
Illumina HumanHT-12 V4.0 expression beadchip
Description
CBL0137 id non-genotoxic DNA binding compounds which directly destabilizes nucleosomes in cells. Effect of different doses of CBL0137 on the abundance of mRNA was studied in two cell types, multiple myeloma MM1.S and cervical carcinoma HeLa cell.
Publication Title
No associated publication
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Compares shFOXO4 vs. Control in LNCaP grown in culture, or in nude mice as primary orthotopic tumors or lymph node metastases
Publication Title
A genome-wide RNAi screen identifies FOXO4 as a metastasis-suppressor through counteracting PI3K/AKT signal pathway in prostate cancer.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 22 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
No associated publication
Sample Metadata Fields
Specimen part, Cell line, Treatment, Time
View Samples- Homo sapiens
- 22 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
To understand the effect of nicotine on sensitivity of cancer cells to radiation or anti-cancer drugs, NCI-H460 human lung large cell carcinoma cells were treated with 6 Gy ionizing radiation or 1 uM cisplatin after exposure to 5 uM nicotine or cigarette smoke extract. Whole genome expression in total RNA extracted from the treated cells was quantified using the GeneChip Human Gene 1.0 ST microarray platform from Affymetrix (Santa Clara, CA).
Publication Title
No associated publication
Sample Metadata Fields
Specimen part, Cell line, Treatment, Time
View Samples- Homo sapiens
- 51 Downloadable Samples
- Affymetrix Human Genome U95 Version 2 Array (hgu95av2)
Description
Time-course and concentration-effect experiments with multiple time points and drug concentrations provide far more valuable information than experiments with just two design-points (treated vs. control), as commonly performed in most microarray studies. Analysis of the data from such complex experiments, however, remains a challenge. Here we present a semi-automated method for fitting time profiles and concentration-effect patterns, simultaneously, to gene expression data. The submodels for time-course included exponential increase and decrease models with parameters such as initial expression level, maximum effect, and rate-constant (or half-time). The submodel for concentration-effect was a 4-parameter Hill model.
Publication Title
Simultaneous modeling of concentration-effect and time-course patterns in gene expression data from microarrays.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 11 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Dendritic cells (DC) arise from a diverse group of hematopoietic progenitors and have marked phenotypic and functional heterogeneity. We have found previously that activation of protein kinase C beta 2 (PRKCB2) by cytokines or phorbol esters drives normal human CD34(+) hematopoietic progenitors and myeloid leukemic blasts (KG1, K562 cell lines, and primary patient blasts) to differentiate into DC, but the genetic program triggered by PRKCB2 activation that results in DC differentiation is only beginning to be characterized. Of the cPKC isoforms, only PRKCB2 was consistently activated by DC differentiation-inducing stimuli in normal and leukemic progenitors. To examine early changes in gene expression following PRKCB2 activation, we employed the following cell lines: (1) the CD34(+) human acute myeloid leukemia derived cell line KG1, which undergoes DC differentiation following phorbol ester treatment; (2) KG1a, a spontaneously arising differentiation-resistant daughter cell line of KG1 that has lost PRKCB2 expression; (3) clones established from KG1a that stably express exogenous PRKCB2-GFP fusion proteins and are once again able to undergo DC differentiation (KG1a-PRKCB2-GFP Clone E9 and Clone E11). We examined changes in gene expression in these cells following treatment with the phorbol ester PMA (phorbol 12-myristate 13-acetate) for 2 hours. Since KG1 and KG1a differ in PRKCB2 expression but have similar expression of the other protein kinase C isoforms, this protocol will allow for the identification of genes regulated by PRKCB2 activation.
Publication Title
Tumor-induced STAT3 signaling in myeloid cells impairs dendritic cell generation by decreasing PKCβII abundance.
Sample Metadata Fields
Sex, Age, Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
FACT inhibition, via small molecule or shRNA, lead to reduced growth and viability of all BrCa cells tested. Phenotypic changes were more severe in high FACT cells (death or growth arrest) than in low FACT cells (decreased proliferation). Though inhibition had no effect on the rate of general transcription, expression of individual genes was changed in a cell-specific manner. Initially distinct transcriptional profiles of BrCa cells became almost identical via equalizing FACT expression. We found that in high-FACT cells FACT supports expression of genes involved in the regulation of cell cycle, DNA replication, maintenance of undifferentiated cell state and regulated by the activity of proto-oncogenes, such as Hras, cMyc, E2F family ets. In low-FACT cells presence of FACT reduces expression of genes coding enzymes of steroid metabolism characteristic for the differentiated mammary epithelia. Inhibition of FACT leads to the shift from more aggressive transcriptional program to more benign, accompanied with similar type of phenotypical changes. Thus we propose FACT as a marker to predict aggressiveness of BrCa and as a target to either kill aggressive BrCa cells or to convert them to a less aggressive phenotype.
Publication Title
No associated publication
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Inhibition of the nonsense mediated decay (NMD) mechanism in cells results in stabilization of transcripts carrying premature translation termination codons. A strategy referred to as gene indentification by NMD inhibition (GINI) has been proposed to identify genes carrying nonsense mutations (Noensie & Dietz, 2001). Genes containing frameshift mutations in colon cancer cell line have been identifying mutatnt genes using GINI, we have now further improved the strategy. In this approach, inhibition of NMD with emetine is complemented with inhibiting NMD by blocking the phosphorylation of the hUpf1 protein with caffeine. In addition, to enhance the GINI strategy, comparing mRNA level alterations produced by inhibiting transcription alone or inhbiiting transcription together with NMD following caffeine pretreatment were used for the efficient identification of false positives produced as a result of stress response to NMD inhibition. To demonstrate the improved efficiency of this approach, we analyzed colon cancer cell lines showing microstellite instability. Bi-allelic inactivating mutations were found in the FXR1, SEC1L1, NCOR1, BAT3, PHD14, ZNF294, C190ORF5 genes as well as genes coding for proteins with yet unknown functions.
Publication Title
Identifying candidate colon cancer tumor suppressor genes using inhibition of nonsense-mediated mRNA decay in colon cancer cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We used a modification of GINI analysis to identify genes containing premature translation termination codons (PTC) generated by nonsense or frameshift mutations in prostate cancer cell lines. The analysis was performed in two steps. In the first step nonsense mediated mRNA decay (NMD) was inhibited in prostate cancer cell lines using incubation with medium containing caffeine for 4 hours. Gene expression analysis of caffeine treated or untreated cells after this step detects mRNA accumulation that takes place for genes containing PTC and as well as for genes that show induction of transciption due to stress caused by NMD inhibition. In the second step either both transcription and NMD or transcription only are blocked by incubating cell in a medium containing either both actinomycin D and caffeine or actinomacin D only for 4 hours. Gene expression analysis after this second step detects mRNA degradation for genes containing PTC as well as for genes that show induction of transciption due to stress caused by NMD inhibition. The efficiency of mRNA degradation for genes containing PTC during this step depends on whether NMD is inhibited or not. The efficiency of mRNA degradation for stress response genes does not depend on whether NMD is inhibited or not.
Publication Title
Par-3 partitioning defective 3 homolog (C. elegans) and androgen-induced prostate proliferative shutoff associated protein genes are mutationally inactivated in prostate cancer cells.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
It has been shown that retinoic acid (RA) can both inhibit and promote cancer cell growth, but the basis of this paradox is still not clear. The action of RA is mainly mediated by RA receptors (RARs), which classically function as ligand-activated transcription factors. Upon binding to the RA receptor alpha (RARA), RA modulates the transcription of several RA-target genes involved in multiple cellular processes, including cell proliferation. We have found that functional inhibition of RARA transcriptional function by stable expression of a RARA dominant negative (RARA403) converts T47D breast cancer cells from growth-inhibited to growth-promoted by supraphysiological RA (Ren et al., MCB, 2005, PMID:16287870; Somenzi et al., PloS ONE, 2007, PMID:17786207). We hypothesized that RA-induced cell growth requires both the activation of RA-responsive tumor-promoting signalings and lack of activation of RA-responsive tumor suppressor signalings. To identify these signalings, we analyzed the transcriptional response to RA in our model of the RA paradox by using gene expression microarrays.
Publication Title
No associated publication
Sample Metadata Fields
Cell line, Treatment
View Samples