We analyzed transcriptional changes in 4 prostate cancer cell lines following treatment with the BET inhibitor I-BET762 using Affymetrix Human Genome U133 Plus 2.0 Arrays.
Inhibition of BET bromodomain proteins as a therapeutic approach in prostate cancer.
Cell line, Time
View SamplesTranscriptional changes were analyzed in two colorectal cancer, two pancreatic cancer, and one small cell lung cancer cell line following treatment with the BET inhibitor GSK525762 and/or the MEK inhibitor trametinib using Affymetrix Human Genome U133 Plus 2.0 Arrays.
MEK inhibitors overcome resistance to BET inhibition across a number of solid and hematologic cancers.
Cell line, Treatment, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
EZH2 inhibition as a therapeutic strategy for lymphoma with EZH2-activating mutations.
Specimen part, Cell line, Treatment
View SamplesWe studied transcriptional changes by Affymetrix human microarrays in DLBCL cell lines as a result of treatment with GSK126, a potent, highly-selective, SAM-competitive, small molecule inhibitor of EZH2
EZH2 inhibition as a therapeutic strategy for lymphoma with EZH2-activating mutations.
Specimen part, Cell line, Treatment
View SamplesWe studied transcriptional changes by Affymetrix human microarrays in 2 DLBCL cell lines as a result of shRNA mediated knockdown of EZH2.
EZH2 inhibition as a therapeutic strategy for lymphoma with EZH2-activating mutations.
Specimen part, Cell line, Treatment
View SamplesPurpose: The goal of this study was to map the pathway of mRNA decay by human RNase L Methods: Total RNA was extracted (RNeasy kit, Qiagen). RNA integrity was verified by an RNA 6000 Nano Chip, using BioAnalyzer and 2100 Expert software (Agilent Technologies). The mRNA was enriched by oligo-dT pulldown from total RNA, followed by fragmentation, adapter ligation, PCR amplification, and finally sequencing on Illumina HiSeq 2000 platform. For sequencing introns, the oligo-dT pulldown step was replaced with Ribo-Zero rRNA removal (Illumina). Sequencing reads were mapped to the human genome hg19 using TopHat 2 set to map stranded reads with default parameters. Mapped read counts were obtained using HTseq-count run in union mode. Results: We developed an approach for transcriptome-wide profiling of RNase L activity in human cells and identified hundreds of direct RNA targets and non-targets. We show that this RNase L-dependent decay (RLDD) selectively affects transcripts regulated by miR-17/miR-29/miR-200 and other microRNAs that function as suppressors of mammalian cell adhesion and proliferation. RNase L mimics the effects of these microRNAs and acts as a suppressor of proliferation and adhesion in mammalian cells. Conclusions: Our data suggest that RLDD serves to establish an anti-proliferative state via destabilization of the microRNA-regulated transcriptome. Overall design: Human mRNA profiles from HeLa, T47D and HAP1 cells were generated by deep sequencing using Illumina Illumina HiSeq 2000.
Human RNase L tunes gene expression by selectively destabilizing the microRNA-regulated transcriptome.
No sample metadata fields
View SamplesThe germinal center (GC) is a microanatomical compartment wherein high-affinity antibody-producing B cells are selectively expanded. B cells proliferate and mutate their antibody genes in the dark zone (DZ) of the GC and are then selected by T cells in the light zone (LZ) on the basis of affinity. Here, we show that T cell help regulates the speed of cell cycle phase transitions and DNA replication of GC B cells. Genome sequencing and single-molecule analyses revealed that T cell help shortens S phase by regulating replication fork progression while preserving the relative order of replication origin activation. Thus, high-affinity GC B cells are selected by a mechanism that involves prolonged dwell time in the DZ where selected cells undergo accelerated cell cycles. Overall design: To determine whether GC B cells receiving high levels of T cell help show a specific change in gene expression, we compared DZ cells in the G1 phase of the cell cycle from aDEC-OVA and control aDEC-CS treated GCs using a fluorescent ubiquitination-based cell cycle indicator (Fucci-tg). RNA sequencing revealed that T cell-mediated selection produced an increase in gene expression programs associated with the cell cycle, metabolism, including the metabolism of nucleotides, and genes downstream of c-Myc and the E2F transcription factors.
HUMORAL IMMUNITY. T cell help controls the speed of the cell cycle in germinal center B cells.
No sample metadata fields
View SamplesWhole-transcriptome survey of gene expression differences between germ-free (GF) and conventionally raised (CONV-R) mice.
Analysis of gut microbial regulation of host gene expression along the length of the gut and regulation of gut microbial ecology through MyD88.
Specimen part
View SamplesmRNA regulation by the circadian protein Nocturnin in A549 cells. Overall design: Total RNA from WT and NOCT KO A549 cells were subject to poly-A pulldown and RNA-seq.
The metabolites NADP<sup>+</sup> and NADPH are the targets of the circadian protein Nocturnin (Curled).
Cell line, Subject
View SamplesWe investigated the molecular mechanisms for osteolytic bone metastasis by selecting human lung cancer cell line subpopulations with elevated metastatic activity and validating genes that are overexpressed in these cells. A bone-seeking squamous lung cancer cell line (HARA-B4) was established by sequentially injecting parental HARA cells into the left ventricle of male 5-week-old nude mice 4 times.
Involvement of CXCL14 in osteolytic bone metastasis from lung cancer.
Specimen part, Cell line
View Samples