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accession-icon GSE78698
Targeting metabolic symbiosis to overcome resistance to anti-angiogenic therapy
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Despite the approval of several anti-angiogenic therapies, clinical results remain unsatisfactory, and transient benefits are followed by rapid tumor recurrence. In the present study, we aimed to identify resistance mechanisms to the small-molecule tyrosine kinase inhibitor nintedanib in the Py2T murine breast cancer transplantation model. To identify differences in gene expression between short- and long-term nintedanib and untreaded FAC-sorted tumor and endothelial cells, we performed gene expression profiling by using affymetrix microarrays.

Publication Title

Targeting Metabolic Symbiosis to Overcome Resistance to Anti-angiogenic Therapy.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP044099
The contribution of cohesin-SA1 to chromatin architecture and gene expression in two murine tissues
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Cohesin, which consists of SMC1, SMC3, Rad21 and either SA1 or SA2, topologically embraces the chromatin fibers to hold sister chromatids together and to stabilize chromatin loops. Increasing evidence indicates that these loops are the organizing principle of higher-order chromatin architecture, which in turn is critical for gene expression. To determine how cohesin contributes to the establishment of tissue-specific transcriptional programs, we compared genome-wide cohesin distribution, gene expression and chromatin architecture in cerebral cortex and pancreas from adult mice. More than one third of cohesin binding sites differ between the two tissues and these are enriched at the regulatory regions of tissue-specific genes. Cohesin colocalizes extensively with the CCCTC-binding factor (CTCF). Cohesin/CTCF sites at active enhancers and promoters contain, at least, cohesin-SA1 whereas either cohesin-SA1 or cohesin-SA2 are present at active promoters independently of CTCF. Analyses of chromatin contacts at the Protocadherin gene cluster and the Regenerating islet-derived (Reg) gene cluster, mostly expressed in brain and pancreas respectively, revealed remarkable differences in the architecture of these loci in the two tissues that correlate with the presence of cohesin. Moreover, we found decreased binding of cohesin and reduced transcription of the Reg genes in the pancreas of SA1 heterozygous mice. Given that Reg proteins are involved in the control of inflammation in pancreas, such reduction may contribute to the increased incidence of pancreatic cancer reported in these animals. Overall design: Examination of the relationship between gene expression, genome wide cohesin distribution and chromatin structure

Publication Title

The contribution of cohesin-SA1 to gene expression and chromatin architecture in two murine tissues.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP132298
Targeting CREBBP/EP300 bromodomains in cancer
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Changes in gene expression caused by CREBBP/EP300 bromodomain inhibitors in a CML cell line Overall design: K562 cells were treated with CBP30 and I-CBP112 and changes in gene expression were evaluated by RNA-seq

Publication Title

CREBBP/EP300 bromodomains are critical to sustain the GATA1/MYC regulatory axis in proliferation.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon SRP068961
Targeting CREBBP/EP300 in cancer
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Antiprolifereative effects of CREBBP/EP300 inhibitors were tested in human leukemia and lymphoma cell lines and the molecular mechanisms responsible for such effects were explored. Overall design: K562 cells were treated with CBP-30 (CREBBP/EP300 bromodomain inhibitor), C646 (CREBBP/EP300 HAT activity inhibitor) and JQ1 (BRD4 inhibitor) and changes in gene expression were evaluated by RNA-seq.

Publication Title

CREBBP/EP300 bromodomains are critical to sustain the GATA1/MYC regulatory axis in proliferation.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP064155
Nuclear RNA in the nervous system
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Background: Recent characterization of the transcriptional landscape of cell lines and whole tissues has suggested widespread transcription of the genome, including loci that produce regulatory non-coding RNAs that function within the nucleus. Methods: Here, we have defined the nuclear transcriptional landscape of the three major cellular divisions of the nervous system using flow sorting of genetically labeled nuclei from bacTRAP mouse lines followed by characterization the unique expression of coding, non-coding and intergenic RNAs in the mature mouse brain with RNAseq, and validation with independent methods. Results: Our findings reveal diverse expression across the cell-types of all classes of RNAs, including long non-coding RNAs - several of which were confirmed as highly enriched in the nuclei of specific cell-types using anatomical methods. Finally, we also discovered several examples of cell-type specific expression of tandem gene fusions, and report the first cell-type specific expression of circular RNAs, notably a neuron specific and nuclear enriched RNA arising from the gene Hnrnpu. Conclusion: These non-coding RNA expression data should provide an important context for studies evaluating the function of a variety of ncRNA in the nervous system. Overall design: Three to four independent replicate samples (each from one mouse) were collected for each of three sample types: Neuronal nuclear RNA, Astrocyte nuclear RNA, Oligodendrocyte nuclear RNA. Controls include low-coverage presorted nuclear RNA from each mouse.

Publication Title

A Comprehensive Analysis of Cell Type-Specific Nuclear RNA From Neurons and Glia of the Brain.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon GSE18003
Skin Electrovaccination: Effects on Transgene Expression, DNA Persistence and Local Tissue Environment
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Background: The use of electrical pulses to enhance uptake of molecules into living cells have been used for decades. This technique, often referred to as electroporation, has become an increasingly popular method to enhance in vivo DNA delivery for both gene. therapy applications as well as for delivery of vaccines against both infectious diseases and cancer. In vivo electrovaccination is currently being investigated in several clinical trials, including DNA delivery to healthy volunteers. However, the mode of action at molecular level is not yet fully understood.

Publication Title

Skin electroporation: effects on transgene expression, DNA persistence and local tissue environment.

Sample Metadata Fields

Specimen part

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accession-icon SRP064418
Effects of NSD2 depletion on gene expression and H3K36me2 in a lung cancer cell line
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

The histone methyltransferase NSD2/WHSC1/MMSET is overexpressed in a number of solid tumors but its contribution to the biology of these tumors is not well understood. Here, we describe that NSD2 contributes to the proliferation of a subset of lung cancer cell lines by supporting oncogenic RAS transcriptional responses. Co-treatment with MEK and BRD4 inhibitors causes co-operative inhibitory responses on cell growth. While these inhibitors converge in the downregulation of genes associated with cancer-acquired super-enhancers, NSD2 inhibition complements their action by affecting the expression of clusters of genes embedded in megabase-scale regions marked with H3K36me2. Thus, combinatorial therapies using MEK or BRD4 inhibitors together with NSD2 inhibition ensure a more comprehensive inhibition of oncogenic RAS-driven transcription programs. Overall design: H1299 cells were transduced with doxycycline (dox) inducible shRNAs (sh3 or sh5) againts NSD2 and with non target shRNA (shNT). Changes in gene expression (RNA-seq) and H3K36me2 (ChIP-seq) caused by depletion of NSD2 and indicated treatments were assessed. Two replicates (Rep) for RNA-seq and three replicates for ChIP-seq were included.

Publication Title

NSD2 contributes to oncogenic RAS-driven transcription in lung cancer cells through long-range epigenetic activation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE38031
DNA damage-induced differentiation of NSC
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Murine ES-derived neural stem cells (NSC) were not irradiated (ctrl) or irradiated with 10Gy and cultured for 7 days (irr).

Publication Title

DNA damage in mammalian neural stem cells leads to astrocytic differentiation mediated by BMP2 signaling through JAK-STAT.

Sample Metadata Fields

Specimen part

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accession-icon GSE19352
Activation of phosphatidylcholine-cycle enzymes in human epithelial ovarian cancer cells
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Altered phosphatidylcholine (PC) metabolism in epithelial ovarian cancer (EOC) can provide choline-based imaging approaches as powerful tools to improve diagnosis and identify new therapeutic targets. Biochemical, protein and mRNA expression analyses demonstrated that the increase in the major choline-containing metabolite phosphocholine (PCho) in EOC compared with normal and non-tumoral immortalized counterparts (EONT) mainly rely upon: 1) ChoK activation, consistent with higher protein content and increased ChoKalpha mRNA expression levels; 2) PC-plc activation, consistent with higher, previously reported, protein expression. More limited and variable sources of PCho could derive, in some EOC cells, from activation of Phospholipase D or GPC-pd. Phospholipase A2 activity and isoforms expression levels were lower or unchanged in EOC compared with EONT cells. Increased ChoKalpha mRNA, as well as ChoK and PC-plc protein expression, were also detected in surgical specimens isolated from EOC patients. Overall, we demonstrated that the elevated PCho pool detected in EOC cells primarily resulted from the upregulation/activation of ChoK and PC-plc involved in the biosynthetic and in a degradative pathway of the PC-cycle, respectively.

Publication Title

Activation of phosphatidylcholine cycle enzymes in human epithelial ovarian cancer cells.

Sample Metadata Fields

Age, Specimen part, Disease stage, Cell line

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accession-icon SRP026667
Genes regulated in mouse liver by expressing ectopically hURI in hepatocytes
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

RNA-seq was performed using the RNA extracted from the bottom half of right lobe of mouse livers. Mice fall into two groups, mutant group which express ectopic hURI and their control littermates which do not express hURI. Two time points were considered in the study, 1-week-old mice, expressing hURI since 1 week (n =3, 4 for control and mutant, respectively) and 8-week-old mice expressing hURI since 8 week (n= 4, 3 for control and mutant, respectively), as hURI is expressed since conception. Overall design: Determination of differentially expressed transcripts over two time points (1 week and 8 weeks) in mouse livers expressing hURI (1 week and 8 weeks).

Publication Title

Inhibition of de novo NAD(+) synthesis by oncogenic URI causes liver tumorigenesis through DNA damage.

Sample Metadata Fields

Specimen part, Subject

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...

refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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