Filters
Technology
Platform
GSE41972
Homo sapiens
6 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Numerous studies have described the altered expression and the causal role of miRNAs in human cancer. However, to date efforts to modulate miRNA levels for therapeutic purposes have been challenging to implement. Here, we find that Nucleolin (NCL), a major nucleolar protein, post-transcriptionally regulates the expression of a specific subset of miRNAs, including miR-21, miR-221, miR-222, and miR-103, causally involved in breast cancer initiation, progression and drug-resistance. We also show that NCL is commonly overexpressed in human breast tumors, and its expression correlates with that of NCL-dependent miRNAs. Finally, this study indicates that NCL-binding guanosine-rich aptamers affect the levels of NCL-dependent miRNAs and their target genes, reducing breast cancer cell aggressiveness, both in vitro and in vivo. These findings illuminate a path to novel therapeutic approaches based on NCL-targeting aptamers for the modulation of miRNA expression in the treatment of breast cancer.
Publication Title
In vivo NCL targeting affects breast cancer aggressiveness through miRNA regulation.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 18 Downloadable Samples
- Affymetrix Human Transcriptome Array 2.0 (hta20)
Description
EGFR tyrosine kinase inhibitors cause dramatic responses in EGFR-mutant lung cancer, but resistance universally develops. The involvement of -catenin in EGFR TKI resistance has been previously reported however the precise mechanism by which -catenin activation contributes to EGFR TKI resistance is not clear. Here, we show that EGFR inhibition results in the activation of -catenin signaling in a Notch3-dependent manner, which facilitates the survival of a subset of cells that we call adaptive persisters. We previously reported that EGFR-TKI treatment rapidly activates Notch3, and here describe the physical association of Notch3 with -catenin, leading to increased stability and activation of -catenin. We demonstrate that the combination of EGFR-TKI and a -catenin inhibitor inhibits the development of these adaptive persisters, decreases tumor burden, improves recurrence free survival, and overall survival in xenograft models. These results supports combined EGFR-TKI and -catenin inhibition in patients with EGFR mutant lung cancer.
Publication Title
Notch3-dependent β-catenin signaling mediates EGFR TKI drug persistence in EGFR mutant NSCLC.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 3 Downloadable Samples
Illumina HiSeq 2500
Description
We performed single-cell RNA-seq on CD4 T cells isolated from the tonsils of one healthy donor. We used the 10x chromium technology. Overall design: Tonsil CD4 T cells were enriched by negative selection using magnetic beads. Cell populations (CXCR5+PD-1low T cells, CXCR5+PD-1int T cells and CXCR5+PD-1high T cells ) were further isolated by cell sorting. Cellular suspensions (3500 cells) were loaded on a 10X Chromium instrument (10X Genomics) according to manufacturer's protocol.
Publication Title
Human lymphoid organ cDC2 and macrophages play complementary roles in T follicular helper responses.
Sample Metadata Fields
Subject
View Samples- Homo sapiens
- 1 Downloadable Sample
- Illumina HiSeq 2500
Description
We performed single-cell RNA-seq on CD14+ cells isolated from the tonsils of one healthy donor. We used the 10x chromium technology. Overall design: Tonsil phagocytes were prepared by centrifugation on a Ficoll gradient. Dendritic cells and macrophages were enriched by negative selection using magnetic beads. Cell populations were further isolated by cell sorting. Cellular suspensions (3500 cells) were loaded on a 10X Chromium instrument (10X Genomics) according to manufacturer's protocol.
Publication Title
Human lymphoid organ cDC2 and macrophages play complementary roles in T follicular helper responses.
Sample Metadata Fields
Subject
View Samples- Mus musculus
- 40 Downloadable Samples
- Illumina HiSeq 2500
Description
We report RNA sequencing data from tenocytes treated with IGF1. Tenocytes were obtained from the tail tendons of adult C57Bl/6 mice via collagenase digestion. Tenocytes were grown to 60% confluence, and then treated with 100ng/mL of recombinant IGF1 for a period of 0, 1, 2, 6, or 24 hours. Experiments were conducted in quadruplicate. RNA was isolated and prepared for RNA sequencing. Overall design: Differential expression of mRNAs were evaluated from tenocytes isolated from tail tendons of adult wild type C57Bl/6 mice that were treated with recombinant IGF1 for 0, 1, 2, 6, and 24 hours.
Publication Title
Insulin-like growth factor 1 signaling in tenocytes is required for adult tendon growth.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 22 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Plasmodium berghei ANKA infection in mice is used as a model for human cerebral malaria, the most severe complication of Plasmodium falciparum infection. The response of brain cells such as microglia has been little investigated, and may play a role in the pathogenesis or regulation of cerebral malaria. We showed previously that microglia are activated in P. berghei infections, and that Type 1 Interferon signaling is important for activation. This dataset contains the transcriptome of brain microglia of infected mice in the presence and absence of Type I interferon signaling, with the aim of identifying the genes involved in this pathway in microglia during experimental cerebral malaria. Refererence: Capuccini et al 2016, Scientific Reports, 6:39258
Publication Title
Transcriptomic profiling of microglia reveals signatures of cell activation and immune response, during experimental cerebral malaria.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples- Mus musculus
- 10 Downloadable Samples
- Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
Platelet-derived growth factor receptor (PDGFR) signaling plays an important role in the embryonic formation of many different tissues. There is a family of PDGF isoforms which signal through the PDGF receptors (PDGFR) and (PDGFR). PDGF regulates many key cellular processes of mesenchymal cell function including proliferation, differentiation, migration and extracellular matrix (ECM) synthesis. While PDGF has been used to enhance flexor tendon healingin vivo, its role in postnatal tendon growth has remained largely unexplored. To determine the importance of PDGFR signaling in postnatal tendon growth, we performed pharmacological blockade of PDGFR and PDGFR, and then induced tendon growth via mechanical overload using the hindlimb synergist ablation model. Our hypothesis was that inhibition of PDGFR signaling will restrict normal growth of tendon tissue in response to mechanical loading.
Publication Title
Postnatal tendon growth and remodeling require platelet-derived growth factor receptor signaling.
Sample Metadata Fields
Sex, Treatment
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
Genetic disruption of thioredoxin reductase 1 protects against acetaminophen (APAP) toxicity.
Publication Title
A Txnrd1-dependent metabolic switch alters hepatic lipogenesis, glycogen storage, and detoxification.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
DIDO as a Switchboard that Regulates Self-Renewal and Differentiation in Embryonic Stem Cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Transition from symmetric to asymmetric cell division requires precise coordination of differential gene expression. Embryonic stem cells (ESC) strongly express Dido3, whose C-terminal truncation impedes ESC differentiation while retaining self-renewal. We show that Dido3 binds to its gene locus via H3K4me3 and RNA pol II and, at differentiation onset, induces expression of its splice variant Dido1, which then leads to Dido3 degradation and downregulation of stemness genes. We propose that Dido isoforms act as a switchboard to regulate genetic programs for ESC transition from pluripotency maintenance to promotion of differentiation.
Publication Title
DIDO as a Switchboard that Regulates Self-Renewal and Differentiation in Embryonic Stem Cells.
Sample Metadata Fields
Specimen part
View Samples