The data was used to study mechanisms of apoptosis resistance induced by loss of PRC2. Overall design: CCRF-CEM cells infected with shLuciferase, shGFP, shEZH2.1, shEZH2.4, shEED2, shEED5, shSUZ12.2, shSUZ12.3 were harvested, RNA isolated, and RNAsequencing performed on HiSeq 2000.
PRC2 loss induces chemoresistance by repressing apoptosis in T cell acute lymphoblastic leukemia.
Cell line, Subject
View SamplesRNAseq (3''DGE) profiles of osteoblasts from four lung cancer-bearing mice and three tumor-free mice. Overall design: Osteoblasts were FACS-sorted using the following markers: CD45-CD31-Terr119-GFP+ from lineage depleted bone and bone marrow tissue of lung tumor-bearing or tumor-free age-, sex- and litter-matched KrasLSL-G12D/WT;p53Flox/Flox (KP)-Ocn GFP mice. Total RNA was prepared using the Trizol method followed cDNA preparation, amplification, Illumina adapter ligation and 3''end sequencing by Illumina HiSeq 2500
Osteoblasts remotely supply lung tumors with cancer-promoting SiglecF<sup>high</sup> neutrophils.
Sex, Age, Specimen part, Subject
View SamplesTime course micro array experiment to identify transcriptional changes in response to exposure of hFLs to different combinations of small molecules during direct neuronal reprogramming
Small molecules increase direct neural conversion of human fibroblasts.
Specimen part, Treatment, Time
View SamplesTranscriptomic studies revealed that hundreds of mRNAs show differential expression in the brains of sleeping versus awake rats, mice, flies, and sparrows. Although these results have offered clues regarding the molecular consequences of sleep and sleep loss, their functional significance thus far has been limited. This is because the previous studies pooled transcripts from all brain cells, including neurons and glia.
Effects of sleep and wake on oligodendrocytes and their precursors.
Specimen part
View SamplesComparison of gene expression profile of Ewing sarcoma cells which have an exchange of the endogenous EWS/FLI1 to either wild-type or a turnover-deficient mutant EWS/FLI1. Most target genes are saturated as only a few target genes are soly driven by increasing protein amount.
Proteasomal Degradation of the EWS-FLI1 Fusion Protein Is Regulated by a Single Lysine Residue.
No sample metadata fields
View SamplesAlthough recent studies support regenerative potential based on cardiac progenitor cells (CPCs), it remains unclear what cues regulate CPC fate. Using 2- and 3D-culture models, we demonstrate that the two most abundantly expressed matrix proteins in the heart, laminin and fibronectin, have opposite roles in CPC fate decision. CPCs on fibronectin showed predominantly nuclear localization of the transcriptional co-activator YAP and maintained proliferation. In contrast, seeding on laminin induced cytosolic retention and degradation of YAP and altered gene expression, which preceded decreased proliferation and enhanced lineage commitment. RNA-sequencing identified Plk2 as candidate target gene of YAP. Plk2 expression depended on YAP stability, was rapidly downregulated on laminin, and its regulation was sufficient to rescue and/or mimic the CPC response to laminin and fibronectin, respectively. These findings propose a novel role of Plk2 and identify an early molecular mechanism in matrix-instructed CPC fate with potential implications for therapeutic cardiac regeneration. Overall design: Expression profiling of cardiac progenitor cells in suspension and cultured on dishes coated with laminin or fibronectin or on non-coated dishes (biological triplicates each)
Polo-Like Kinase 2 is Dynamically Regulated to Coordinate Proliferation and Early Lineage Specification Downstream of Yes-Associated Protein 1 in Cardiac Progenitor Cells.
No sample metadata fields
View SamplesPaired-end sequencing of Vector and H-Ras expressing cell lines: p53-del and WT-p53 We found that activated forms of H-Ras and PIK3CA oncogene lead to repression of p63, a p53 family member. They also lead to induction of EMT, a cancer-related process. Our results suggest that, through Ras regulation of p63, this oncogene can drive mammary epithelial cells towards greater invasive ability. Overall design: 4 samples analyzed with 3 replicates each, control samples for each H-Ras line are the Vector cell line created at the same time
Repression of p63 and induction of EMT by mutant Ras in mammary epithelial cells.
Cell line, Subject
View SamplesThe intermediate filament protein Nestin serves as a biomarker for stem cells and has been used to identify subsets of cancer stem-like cells. However, the mechanistic contributions of Nestin to cancer pathogenesis are not understood. Here we report that Nestin binds the hedgehog pathway transcription factor Gli3 to mediate the development of medulloblastomas of the hedgehog subtype. In a mouse model system, Nestin levels increased progressively during medulloblastoma formation resulting in enhanced tumor growth. Conversely, loss of Nestin dramatically inhibited proliferation and promoted differentiation. Mechanistic investigations revealed that the tumor-promoting effects of Nestin were mediated by binding to Gli3, a zinc finger transcription factor that negatively regulates hedgehog signaling. Nestin binding to Gli3 blocked Gli3 phosphorylation and its subsequent proteolytic processing, thereby abrogating its ability to negatively regulate the hedgehog pathway. Our findings show how Nestin drives hedgehog pathway-driven cancers and uncover in Gli3 a therapeutic target to treat these malignancies.
Nestin Mediates Hedgehog Pathway Tumorigenesis.
Specimen part
View SamplesComparison between cell lines from 9 different cancer tissue of origin types (Breast, Central Nervous System, Colon, Leukemia, Melanoma, Non-Small Cell Lung, Ovarian, Prostate, Renal) from NCI-60 panel
Exon array analyses across the NCI-60 reveal potential regulation of TOP1 by transcription pausing at guanosine quartets in the first intron.
Sex, Age, Specimen part, Cell line
View SamplesComparison between cell lines from 9 different cancer tissue of origin types (Breast, Central Nervous System, Colon, Leukemia, Melanoma, Non-Small Cell Lung, Ovarian, Prostate, Renal) from NCI-60 panel.
Topoisomerase I levels in the NCI-60 cancer cell line panel determined by validated ELISA and microarray analysis and correlation with indenoisoquinoline sensitivity.
Sex, Age, Specimen part, Cell line
View Samples