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accession-icon GSE37955
ERa-dependent E2F transcription can mediate resistance to estrogen deprivation in human breast cancer
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

ERα-dependent E2F transcription can mediate resistance to estrogen deprivation in human breast cancer.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE22533
Breast cancer cells resistant to hormone deprivation maintain an estrogen receptor alpha-dependent, E2F-directed transcriptional program
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

A significant fraction of breast cancers exhibit de novo or acquired resistance to estrogen deprivation. To model resistance to aromatase inhibitor (AI) therapy, long-term estrogen-deprived (LTED) derivatives of MCF-7 and HCC-1428 cells were generated through culture for 3 and 7 months under hormone-depleted conditions, respectively. These LTED cells showed sensitivity to the ER downregulator fulvestrant under hormone-depleted conditions, suggesting continued dependence upon ER signaling for hormone-independent growth. To evaluate the role of ER in hormone-independent growth, LTED cells were treated +/- 1 uM fulvestrant x 48 h before RNA was harvested for gene expression analysis.

Publication Title

ERα-dependent E2F transcription can mediate resistance to estrogen deprivation in human breast cancer.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE69976
Induction of muscle stem cell quiescence by the secreted niche factor Oncostatin M
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Regeneration of skeletal muscle is dependent on the function of tissue-resident muscle stem cells (MuSC), known as satellite cells. MuSC dysfunction is central to muscle pathophysiology, including in age-associated loss of muscle regenerative capacity and congenital disorders such as Duchenne muscular dystrophy. Despite the central role of satellite cells in muscle regeneration, the signals controlling the balance between muscle stem cell quiescence, proliferation, and differentiation remain incompletely understood. Knowledge of the signals that maintain a quiescent state is particularly lacking, yet such cues are crucial to maintaining a stem cell reservoir that can meet the needs of regeneration throughout life. Here we identify Oncostatin M (OSM), a member of the interleukin-6 family of cytokines, as a potent and essential trans-acting regulator of satellite cell quiescence. Key to this discovery is the development of a novel in vivo imaging-based screening strategy allowing identification of proteins that do not induce in vitro proliferation, but instead maintain MuSCs in a non-mitotic state, poised for rapid robust expansion upon transplantation. We demonstrate that OSM induces reversible exit from the cell cycle and induction of a global transcriptional program significantly enriched within a newly established satellite cell quiescence signature. Genetic ablation of the OSM receptor in mice demonstrates that signaling via OSM/R is essential for maintenance of satellite cell quiescence, and for proper skeletal muscle regeneration in vivo. Given that aberrant activation and exhaustion of stem cells is seen in a variety of disorders, OSM constitutes an attractive therapeutic target in muscle disease states.

Publication Title

Induction of muscle stem cell quiescence by the secreted niche factor Oncostatin M.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE17639
The human reticulocyte transcriptome (HG-U133_Plus2.0)
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

RNA from circulating blood reticulocytes was utilized to provide a robust description of genes transcribed at the final stages of erythroblast maturation. After depletion of leukocytes and platelets, Affymetrix HG-U133Plus 2.0 arrays were hybridized with probe from total RNA isolated from blood sampled from 6 umbilical cords and 6 healthy adult humans.

Publication Title

Let-7 microRNAs are developmentally regulated in circulating human erythroid cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE19639
Hyperactivation of PI3K promotes escape from hormone dependence in estrogen receptor-positive breast cancer
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Hyperactivation of phosphatidylinositol-3 kinase (PI3K) promotes escape from hormone dependence in estrogen receptor-positive breast cancer.

Publication Title

Hyperactivation of phosphatidylinositol-3 kinase promotes escape from hormone dependence in estrogen receptor-positive human breast cancer.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP050477
Drug-based modulation of endogenous stem cells promotes functional remyelination in vivo
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Multiple sclerosis involves an aberrant autoimmune response and progressive failure of remyelination in the central nervous system. Prevention of neural degeneration and subsequent disability requires remyelination through the generation of new oligodendrocytes, but current treatments exclusively target the immune system. Oligodendrocyte progenitor cells are stem cells in the central nervous system and the principal source of myelinating oligodendrocytes. These cells are abundant in demyelinated regions of patients with multiple sclerosis, yet fail to differentiate, thereby representing a cellular target for pharmacological intervention. To discover therapeutic compounds for enhancing myelination from endogenous oligodendrocyte progenitor cells, we screened a library of bioactive small molecules on mouse pluripotent epiblast stem-cell-derived oligodendrocyte progenitor cells. Here we show seven drugs function at nanomolar doses selectively to enhance the generation of mature oligodendrocytes from progenitor cells in vitro. Two drugs, miconazole and clobetasol, are effective in promoting precocious myelination in organotypic cerebellar slice cultures, and in vivo in early postnatal mouse pups. Systemic delivery of each of the two drugs significantly increases the number of new oligodendrocytes and enhances remyelination in a lysolecithin-induced mouse model of focal demyelination. Administering each of the two drugs at the peak of disease in an experimental autoimmune encephalomyelitis mouse model of chronic progressive multiple sclerosis results in striking reversal of disease severity. Immune response assays show that miconazole functions directly as a remyelinating drug with no effect on the immune system, whereas clobetasol is a potent immunosuppressant as well as a remyelinating agent. Mechanistic studies show that miconazole and clobetasol function in oligodendrocyte progenitor cells through mitogen-activated protein kinase and glucocorticoid receptor signalling, respectively. Furthermore, both drugs enhance the generation of human oligodendrocytes from human oligodendrocyte progenitor cells in vitro. Collectively, our results provide a rationale for testing miconazole and clobetasol, or structurally modified derivatives, to enhance remyelination in patients. Overall design: RNA sequencing of oligodendrocyte progenitor cells treated with vehicle, miconazole or clobetasol for 0, 2, 6, or 12 hours. Cells were plated 1.5 hours prior to addition of drug.

Publication Title

Drug-based modulation of endogenous stem cells promotes functional remyelination in vivo.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE28580
RNA interference screening identifies the Insulin/IGF-1 receptor pathway as a mechanism of escape from hormone dependence in breast cancer
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

A significant fraction of breast cancers exhibit de novo or acquired resistance to estrogen deprivation.

Publication Title

A kinome-wide screen identifies the insulin/IGF-I receptor pathway as a mechanism of escape from hormone dependence in breast cancer.

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon GSE65417
Expression data from C. elegans wild type, hlh-25 mutant and hlh-29 mutant strains
  • organism-icon Caenorhabditis elegans
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Genome Array (celegans)

Description

In Caenorhabditis elegans, the six proteins that make up the REF-1 family are HES homologs that act in both Notch dependent and Notch-independent pathways to regulate embryonic events. To further our understanding of how the REF-1 family works to coordinate post-embryonic cellular events, we performed transcriptome analysis of HLH-25 and HLH-29 mutant strains.

Publication Title

Genome-wide microarrray analysis reveals roles for the REF-1 family member HLH-29 in ferritin synthesis and peroxide stress response.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP096545
Comparison of translational profiles in Motor Neurons (CHAT), to all neurons (Snap25) in the spinal cord.
  • organism-icon Mus musculus
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Translating ribosome affinity purification (TRAP) was performed on spinal cord dissections pooled from 3-4 mice 21 days post birth that were positive for the eGFP-L10A fusion ribosomal marker protein under the expression of either the Chat promoter (Tg(Chat-EGFP/Rpl10a)DW167Htz) or the Snap25 promoter (Tg(Snap25-EGFP/Rpl10a)JD362Jdd). RNA-sequencing was performed on both TRAP and pre-immunoprecipitation (PreIP) control RNA samples. Overall design: Three replicates of PreIP and TRAP for two transgenic lines.

Publication Title

MicroRNA Profiling Reveals Marker of Motor Neuron Disease in ALS Models.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP150320
Next generation sequencing on knockdown of AC093323.3 in lung cancer cells
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

In this study we predict functionally important long intergenic non-coding RNAs (lincRNAs) with a role in core essential processes in human. One of the candidate lincRNA, AC093323.3, was experimentally verified to affect cell viability. We performed RNASeq on knockdown of AC093323.3 to further investigate the functional role of this lincRNA. Overall design: RNA profiles of NCI-H460 lung cancer cells after treatment with scrambled siRNAs and AC093323.3-siRNA.

Publication Title

In silico prediction of housekeeping long intergenic non-coding RNAs reveals HKlincR1 as an essential player in lung cancer cell survival.

Sample Metadata Fields

Cell line, 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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