This SuperSeries is composed of the SubSeries listed below.
A common promoter hypomethylation signature in invasive breast, liver and prostate cancer cell lines reveals novel targets involved in cancer invasiveness.
Sex, Disease, Disease stage, Cell line
View SamplesCancer invasion and metastasis is the most morbid aspect of cancer and is governed by different cellular mechanisms than those driving the deregulated growth of tumors. We addressed here the question of whether a common DNA methylation signature of invasion exists in cancer cells from different origins that differentiates invasive from noninvasive cells. We identified a common DNA methylation signature consisting of hyper- and hypomethylation and determined the overlap of differences in DNA methylation with differences in mRNA expression using expression array analyses. A pathway analysis reveals that the hypomethylation signature includes some of the major pathways that were previously implicated in cancer migration and invasion such as TGF beta and ERBB2 triggered pathways. The relevance of these hypomethylation events in human tumors was validated by identification of the signature in several publicly available databases of human tumor transcriptomes. We shortlisted novel invasion promoting candidates and tested the role of four genes from the list C11orf68, G0S2, SHISA2 and TMEM156 in invasiveness using siRNA depletion. Importantly these genes are upregulated in human cancer specimens as determined by immunostaining of human normal and cancer breast, liver and prostate tissue arrays. Since these genes are activated in cancer they constitute a group of targets for specific pharmacological inhibitors of cancer invasiveness.
A common promoter hypomethylation signature in invasive breast, liver and prostate cancer cell lines reveals novel targets involved in cancer invasiveness.
Sex, Disease, Disease stage, Cell line
View SamplesDespite their distinct biology, granulosa cell tumours (GCTs) are treated the same as other ovarian tumours. Intriguingly, a recurring somatic mutation in the transcription factor Forkhead Box L2 (FOXL2) 402C>G has been found in nearly all GCTs examined. This investigation aims to identify the pathogenicity of mutant FOXL2 by studying its altered transcriptional targets. The expression of mutant FOXL2 was reduced in the GCT cell line KGN, and wildtype and mutant FOXL2 were overexpressed in the GCT cell line COV434. Comparisons were made between the transcriptomes of control cells and cells altered by FOXL2 knockdown and overexpression, to detect potential transcriptional targets of mutant FOXL2. Comparisons were made between the transcriptomes of control cells and cells altered by FOXL2 knockdown and overexpression, to detect potential transcriptional targets of mutant FOXL2.
The transcriptional targets of mutant FOXL2 in granulosa cell tumours.
Cell line
View SamplesMany organisms acquired circadian clock system to adapt daily and seasonal environmental changes. Mammals have the master clock in the brains suprachiasmatic nucleus (SCN) that synchronizes other circadian clocks in the peripheral tissues or organs. Plants also have circadian clock in their bodies, but the presence of the tissue-specific functions of circadian clock is remained elusive. The aim of this experiment is to compare tissue-specific gene expression profile using gene expression Microarray.
Tissue-specific clocks in Arabidopsis show asymmetric coupling.
Specimen part, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Temporal expression of microRNA cluster miR-17-92 regulates effector and memory CD8+ T-cell differentiation.
Specimen part
View SamplesDuring acute viral infections, effector CD8+ T cells differentiate into memory precursors or short-lived terminal effectors. miR-17-92a over-expression skews CD8+ effector cells to the terminal differentiation.
Temporal expression of microRNA cluster miR-17-92 regulates effector and memory CD8+ T-cell differentiation.
Specimen part
View SamplesTranslation is a critical cellular process to synthesize proteins from their transcripts. However, translational regulation in antigen-specific T cells in vivo has not been well defined.
Translation is actively regulated during the differentiation of CD8<sup>+</sup> effector T cells.
Sex, Specimen part
View SamplesOur previous study using nude rats revealed that the parental JDCaP xenografts predominantly expressed full-length androgen receptor (AR) whereas the relapsed JDCaP xenografts after castration acquired AR splice variants including AR-V7 and ARv567es. To understand molecular mechanisms underlying the acquisition of AR splice variants in the JDCaP model, we performed microarray analysis using RNA samples of the xenografts without castration (Parent), the relapsed xenografts overexpressing full-length AR and AR-V7 (ARhiV7hi), and the relapsed xenografts expressing ARv567es (ARv567es).
The RNA helicase DDX39B and its paralog DDX39A regulate androgen receptor splice variant AR-V7 generation.
Specimen part
View SamplesPurpose: To compare the transcriptomes of activated CD4 T effector cell populations in the presence and absence of STAT3 at 8 days post-infection using high-throughput RNA sequencing analysis. Methods: Cell sorting of the populations was done using the markers Ly6c and PSGL-1 Overall design: CD4 T cell Ly6c and PSGL-1 population mRNA profiles 8 days post-LCMV infection of wild type (WT) and STAT3fl/fl Cd4cre mice were generated by mRNA sequencing using Illumina HiSeq 2000.
The Interleukin-2-mTORc1 Kinase Axis Defines the Signaling, Differentiation, and Metabolism of T Helper 1 and Follicular B Helper T Cells.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
IDH2 and NPM1 Mutations Cooperate to Activate Hoxa9/Meis1 and Hypoxia Pathways in Acute Myeloid Leukemia.
Specimen part
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