Deregulation of translational control is an obligatory step in oncogenesis; however, this step has not been addressed by prior genomic and transcriptional profiling studies of cancer biology. Here we simulate the translational deregulation found in cancer by ectopically over expressing translation initiation factor eIF4E in primary human mammary epithelial cells; and examine its impact on cell biology and the pattern of ribosomal recruitment to mRNA genome wide. Over expression of eIF4E allows cells to bypass M0 premature growth arrest, but does not confer other malignant properties. However, in concert with hTERT, eIF4E imparts cells with growth and survival autonomy - and profoundly alters the pattern of polyribosome-associated mRNA encoding cell cycle and apoptosis regulators. The translational response to increased eIF4E is not only a unidirectional activation of oncogenic drivers, but also consists of complex intrinsic translational mechanisms that mitigate the acquisition of neoplastic properties.
Eukaryotic translation initiation factor 4E induced progression of primary human mammary epithelial cells along the cancer pathway is associated with targeted translational deregulation of oncogenic drivers and inhibitors.
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TET1 is a maintenance DNA demethylase that prevents methylation spreading in differentiated cells.
Cell line
View SamplesWe report that full length TET1 (TET1-FL) overexpression fails to induce global DNA demethylation in HEK293T cells. The preferential binding of TET1-FL to hypomethylated CpG islands (CGIs) through its CXXC domain leads to its inhibited 5-hydroxymethylcytosine (5hmC) production as methylation level increases. TET1-FL-induced 5hmC accumulates at CGI edges, while TET1 knockdown induces methylation spreading from methylated edges into hypomethylated CGIs. However, TET1 can regulate gene transcription independent of its dioxygenase catalytic function. Thus, our results identify TET1 as a maintenance DNA demethylase that does not purposely decrease methylation levels, but specifically maintains the DNA hypomethylation state of CGIs in adult cells.
TET1 is a maintenance DNA demethylase that prevents methylation spreading in differentiated cells.
Cell line
View SamplesTranscriptomic response of mouse mixed neuron-glial cell cultures to 1,25-dihydroxyvitamin D3
The transcriptomic response of mixed neuron-glial cell cultures to 1,25-dihydroxyvitamin d3 includes genes limiting the progression of neurodegenerative diseases.
Specimen part, Treatment
View SamplesWe used Affymetrix microarrays to investigate gene expression changes in the liver of lean female Zucker rats exposed to a normal diet supplemented with a rosemary extract rich in the diterpenic compound, carnosic acid (CA).
A rosemary extract enriched in carnosic acid improves circulating adipocytokines and modulates key metabolic sensors in lean Zucker rats: Critical and contrasting differences in the obese genotype.
Sex, Specimen part, Treatment, Time
View SamplesRNA-seq was performed after MCF7 cells were treated with S2101, UNC0638, GSK343, depsipeptide alone or in combination with decitabine Overall design: Biological triplicates were performed for a total of 30 samples. Fold change of each gene was calculated by comparing change in expression after inhibitor treatment to expression in the control samples
Transcriptional Selectivity of Epigenetic Therapy in Cancer.
No sample metadata fields
View SamplesRNA-seq was performed after HL60 cells were treated with S2101, UNC0638, GSK343, depsipeptide alone or in combination with decitabine Overall design: Biological triplicates were performed for a total of 30 samples. Fold change of each gene was calculated by comparing change in expression after inhibitor treatment to expression in the control samples
Transcriptional Selectivity of Epigenetic Therapy in Cancer.
No sample metadata fields
View SamplesRNA-seq was performed after YB5 cells were treated with S2101, UNC0638, GSK343, depsipeptide alone or in combination with decitabine Overall design: Biological triplicates were performed for a total of 30 samples. Fold change of each gene was calculated by comparing change in expression after inhibitor treatment to expression in the control samples
Transcriptional Selectivity of Epigenetic Therapy in Cancer.
No sample metadata fields
View SamplesTranscriptomic analyses of the oxygen response of two glioma cell lines at 20% versus 0.3% O2, and 3% vs 0.3% O2 in the presence or absence of serum
Hypoxia-induced expression of VE-cadherin and filamin B in glioma cell cultures and pseudopalisade structures.
Specimen part, Cell line
View SamplesPurpose: To identify transcriptional changes by RNA-seq in tumor samples, before bevacizumab combination treatment and after bevacizumab combination treatment in both responding and non-responding recurrent glioblastoma patients Overall design: Three comparison analyses were further performed: 1.) Paired analysis of pre- and post-treated samples from responding patients; 2.) Comparison of pre-treated samples of responders vs. non-responders; 3.) Paired analysis of pre- and post-treated samples from non-responding patients The sample ''characteristics: batch'' represents a combination of the RNA-extraction date and the library-preparation date for each sample.
Transcriptional changes induced by bevacizumab combination therapy in responding and non-responding recurrent glioblastoma patients.
Sex, Disease, Disease stage, Subject, Time
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