Filters
Technology
Platform
SRP066356
Homo sapiens
15 Downloadable Samples
IlluminaHiSeq2000
Description
We performed whole transcriptome sequencing of human monocytes that were co-cultured with estrogen receptor positive (ER+) or triple-negative (TNBC) breast cancer cell lines and studied the biological responses related to the differential gene activation in both cell types to understand how different cancer cells educate host cells to support tumor growth Overall design: To characterize the differences in macrophage activation under the influence of either ER+ or TNBC breast cancer cells, we cultured freshly isolated human peripheral monocytes with two breast cancer cell lines (T47D, ER+ and MDA-MB-231, TNBC) in an in vitro transwell co-culture assay. The transwell setting allowed us to investigate the effect of soluble mediators on macrophage activation since direct cell contact of these cells was inhibited by a (PET) membrane (pore size 0.4 µm).
Publication Title
Transcriptional profiling of macrophage and tumor cell interactions in vitro.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 10 Downloadable Samples
Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
Tumor-associated blood vessels differ from normal vessels at the morphological and molecular level. Proteins that are only present on tumor vessels may serve as biomarkers and as therapeutic targets for inhibition of angiogenesis in cancer. Comparing the transcriptional profiles of blood vascular endothelium from human invasive bladder cancer and from normal bladder tissue, we found several markers that could serve as novel biomarkers or therapeutic targets.
Publication Title
Endocan is upregulated on tumor vessels in invasive bladder cancer where it mediates VEGF-A-induced angiogenesis.
Sample Metadata Fields
Sex, Disease stage
View Samples- Homo sapiens
- 23 Downloadable Samples
- Affymetrix Human Genome U95 Version 2 Array (hgu95av2)
Description
Organ transplant recipients (OTRs) on Cyclosporine A (CSA) are prone to catastrophic cutaneous squamous cell carcinoma (SCC). Allograft-sparing, cancer-targeting systemic treatments are unavailable. We have shown increased risk for catastrophic SCC in OTRs via CSA-mediated induction of Interleukin-22 (IL-22). Herein, we found CSA drives SCC proliferation and tumor growth through IL-22 and JAK/STAT pathway induction. We in turn inhibited SCC growth with an FDA-approved JAK 1/2 inhibitor, Ruxolitinib. In human SCC cells, greatest proliferative response to IL-22 and CSA treatment occurred in non-metastasizing lines. IL-22 treatment upregulated JAK1 and STAT1/3 in A431 SCC cells. JAK/STAT pathway genes were highly expressed in tumors from a cohort of CSA-exposed OTRs, and in SCC with high risk for metastasis. Compared to immunocompetent SCC, genes associated with innate immunity, response to DNA damage and p53 regulation were differentially expressed in SCC from OTRs. In nude mice engrafted with human A431 cells, IL-22 and CSA treatment increased tumor growth and upregulated IL-22 receptor, JAK1 and STAT 1/3 expression. Ruxolitinib treatment significantly reduced tumor volume and reversed the accelerated tumor growth. CSA and IL-22 exacerbate aggressive behavior in SCC. Targeting the IL-22 axis via selective JAK/STAT inhibition may reduce the progression of aggressive SCC in OTRs, without compromising immunosuppression.
Publication Title
Ruxolitinib inhibits cyclosporine-induced proliferation of cutaneous squamous cell carcinoma.
Sample Metadata Fields
No sample metadata fields
View Samples- Glycine max
- 71 Downloadable Samples
- NextSeq 500
Description
Gene expression of the F1 Hybrids between two soybean parents (NMS4-44-329 and N7103) were compared. Changes in gene expression were correlated with agronomic traits. Overall design: RNA was isolated from leaf matrial harvested from the field in july of 2015. Four replicates were grown at two location in a random complete block design. Each samples is represented from three or four replications form each location
Publication Title
Changes in gene expression between a soybean F1 hybrid and its parents are associated with agronomically valuable traits.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 16 Downloadable Samples
- IlluminaHiSeq2000
Description
To gain insight into the signaling pathway(s) required for ABL1/ABL2-dependent bone metastasis, we evaluated the consequences of single or double inactivation of ABL1 and ABL2 on the transcriptome of breast cancer cells. Double ABL1/ABL2 knockdown was required to decrease the levels of p-CrKL by more than 90%, indicative of inactivation of the endogenous ABL kinases. To examine the consequences of depleting the ABL kinases on the transcriptome of metastatic breast cancer cells we employed next generation sequencing (RNAseq) analysis. We found that 180 genes were significantly down-regulated and 40 genes were significantly up-regulated in ABL1/ABL2 knockdown cells. Overall design: Four samples were analyzed control, Abl single knockdown, Arg single knockdown, Abl/Arg double knockdown. Experiments were performed in triplicate.
Publication Title
ABL kinases promote breast cancer osteolytic metastasis by modulating tumor-bone interactions through TAZ and STAT5 signaling.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 10 Downloadable Samples
- IlluminaHiSeq2000
Description
To gain insight into the signaling pathway(s) required for ABL1/ABL2-dependent non-small cell carcinoma cells metastasis Overall design: Samples were analyzed by pair of either control versus ABL Kinase inhibitor GNF5, Or using scrambled shRNA versus ABL1/ABL2-specific shRNAs.
Publication Title
Inactivation of ABL kinases suppresses non-small cell lung cancer metastasis.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Activating mutations of FGFR3 are found in a high proportion of bladder tumours. The molecular consequences of FGFR3 mutation in urothelial cells and the mechanisms by which mutant FGFR3 may drive bladder tumourigenesis are largely unknown.
Publication Title
Alteration of cell-cell and cell-matrix adhesion in urothelial cells: an oncogenic mechanism for mutant FGFR3.
Sample Metadata Fields
Specimen part
View Samples- Danio rerio
- 72 Downloadable Samples
- IlluminaHiSeq2000
Description
Both embryonic and adult zebrafish Mycobacterium marinum infection studies have contributed to our knowledge of the development and function of tuberculous granulomas, which are typical for mycobacterial pathogenesis. In this review we discuss how transcriptome profiling studies have helped to characterize this infection process and we include new RNA sequencing (RNA-Seq) data that reveals three main phases in the host response to M. marinum during the early stages of granuloma development in zebrafish embryos and larvae. The late-phase response shares common components with the strong and acute host transcriptome response that has previously been reported for S. typhimurium infection in zebrafish embryos. In contrast, the early/mid-phase response to M. marinum infection, characterized by suppressed pro-inflammatory signaling, is strikingly different from the acute response to S. typhimurium infection. Furthermore, M. marinum infection shows a collective and strongly fluctuating regulation of lipoproteins, while S. typhimurium infection has pronounced effects on amino acid metabolism and glycolysis. Overall design: Embryos were infected at 28 hpf by injecting 250 colony forming units of M. marinum Mma20 in 2%PVP into the caudal vein, or mock-injected with PBS/2%PVP. After injections, embryos were transferred into fresh egg water containing 0.003% 1-phenyl-2-thiourea (Sigma-Aldrich) to prevent melanization and incubated at 28°C. After the incubation period, infected and uninfected groups of 30 embryos were snap-frozen in liquid nitrogen and RNA was isolated for Illumina RNAseq analysis. Samples were taken at the following timepoints: 2, 4, 6, 8 hpi and 1, 2, 3, 4, 5 dpi.
Publication Title
Transcriptomic Approaches in the Zebrafish Model for Tuberculosis-Insights Into Host- and Pathogen-specific Determinants of the Innate Immune Response.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 14 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The morphogen and mitogen, Sonic Hedgehog, activates a Gli1-dependent transcription program that drives proliferation of granule neuron progenitors (GNPs) within the external germinal layer of the postnatally developing cerebellum. Medulloblastomas with mutations activating the Sonic Hedgehog signaling pathway preferentially arise within the external germinal layer, and the tumor cells closely resemble GNPs. Atoh1/Math1, a basic helix-loop-helix transcription factor essential for GNP histogenesis, does not induce medulloblastomas when expressed in primary mouse GNPs that are explanted from the early postnatal cerebellum and transplanted back into the brains of nave mice. However, enforced expression of Atoh1 in primary GNPs enhances the oncogenicity of cells overexpressing Gli1 by almost three orders of magnitude. Unlike Gli1, Atoh1 cannot support GNP proliferation in the absence of Sonic Hedgehog signaling and does not govern expression of canonical cell cycle genes. Instead, Atoh1 maintains GNPs in a Sonic Hedgehog-responsive state by regulating genes that trigger neuronal differentiation, including many expressed in response to bone morphogenic protein-4. Therefore, by targeting multiple genes regulating the differentiation state of GNPs, Atoh1 collaborates with the pro-proliferative Gli1-dependent transcriptional program to influence medulloblastoma development.
Publication Title
Atoh1 inhibits neuronal differentiation and collaborates with Gli1 to generate medulloblastoma-initiating cells.
Sample Metadata Fields
Age, Specimen part, Treatment
View Samples- Mus musculus
- 14 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Myc-driven Group 3 medulloblastoma (MB) is the most aggressive tumor among the four subgroups classified by transcriptome, genomic landscape and clinical outcomes. So far in all available mouse Group 3 models, the constitutive ectopic Myc expression was under control of LTR element or other exogenous promoters within the vectors, which were randomly inserted into the genome with multiple copies. Here we are deploying nuclease deficient CRISPR/dCas9-based transactivator that is targeted to promoter DNA sequences by specific guide RNA to force the transcriptional activation of endogenous Myc in p53-/-;cdkn2c-/- neurospheres cells. A combination of three sgRNAs together with dCas9-VP64 induced the highest expression of endogenous Myc. When the targeted cells were transplanted to the cortex of recipients, tumors arose fully recapitulate the Group 3 MB in human. This novel mouse model should significantly strengthen our understanding and treatment of the Myc-driven Group 3 medulloblastoma.
Publication Title
Mouse medulloblastoma driven by CRISPR activation of cellular Myc.
Sample Metadata Fields
Specimen part
View Samples