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accession-icon GSE12870
Regulation of leukemic cell differentiation and retinoid-induced gene expression by statins
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconSentrix Human-6 Expression BeadChip

Description

There is emerging evidence that, beyond their cholesterol lowering properties, statins exhibit important antileukemic effects in vitro and in vivo, but the precise mechanisms by which they generate such responses remain to be determined. We have previously shown that statins promote differentiation of acute promyelocytic leukemia (APL) cells and enhance generation of all-trans-retinoic acid (ATRA)-dependent antileukemic responses. We now provide evidence that statin-dependent leukemic cell differentiation requires engagement and activation of the JNK kinase pathway. In addition, in experiments to define the molecular targets and mediators of statin-induced differentiation we found a remarkable effect of statins on ATRA-dependent gene transcription, evidenced by the selective induction of over 400 genes by the combination of atorvastatin and ATRA. Altogether, our studies identify novel statin molecular targets linked to differentiation, establish that statins modulate ATRA-dependent transcription, and suggest that combined use of statins with retinoids may provide a novel approach to enhance antileukemic responses in APL and possibly other leukemias.

Publication Title

Regulation of leukemic cell differentiation and retinoid-induced gene expression by statins.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE64666
Expression data from bone marrow-derived dendritic cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Dendritic cells are the sentinels of the innate immune system. We used global microarray analysis to identify genes which are regulated by Toll-like receptor signaling pathways.

Publication Title

IRF8 directs stress-induced autophagy in macrophages and promotes clearance of Listeria monocytogenes.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon SRP051401
Human Schlafen 5 (SLFN5) is a Regulator of Motility and Invasiveness of Renal Cell Carcinoma (RCC) Cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

There is some emerging evidence that members of the Schlafen (SLFN) family of proteins mediate antineoplastic responses, but the mechanisms accounting for these effects are not known. We provide evidence that human SLFN5, an interferon (IFN)- inducible member of the family, exhibits key roles in controlling motility and invasiveness of renal cell carcinoma (RCC) cells. Our studies define the mechanism by which this occurs, demonstrating that SLFN5 negatively controls expression of matrix metalloproteinases (MMP)-1 and -13 and several other genes involved in the control of malignant cell motility. Importantly, our data establish that SLFN5 expression correlates with a better overall survival in a large cohort of patients with RCC. The inverse relationship between SLFN5 expression and RCC aggressiveness raises the possibility of developing unique therapeutic approaches in the treatment of RCC, by modulating SLFN5 expression. Overall design: Examination of 2 SLFN5 knockdown cells and 2 controls, in triplicate.

Publication Title

Human Schlafen 5 (SLFN5) Is a Regulator of Motility and Invasiveness of Renal Cell Carcinoma Cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP149944
Transcription profile analysis of wild type and Irf9-/- bone marrow derived macrophages in response to type I and type II interferons
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Host defense by the innate immune system requires the establishment of antimicrobial states allowing cells to cope with microorganisms before the onset of the adaptive immune response. Interferons (IFN) are of vital importance in the establishment of cell-autonomous antimicrobial immunity. Speed is therefore an important attribute of the cellular response to IFN. With much of the antimicrobial response being installed de novo, this pertains foremost to gene expression, the rapid switch between resting-state and active-state transcription of host defense genes. Our results show how mRNA expression changes upon IFNb or IFNg treatment in wild typ and Irf9-/- bone marrow derived macrophages. Overall design: Methods: Bone marrow derived macrophage mRNA of wild-type (WT) and Irf9 knock out mice (IRF9-/-) untreated, as well as 2h IFNb and IFNg treated were generated by deep sequencing, in triplicate, using Illumina sequencing.

Publication Title

A molecular switch from STAT2-IRF9 to ISGF3 underlies interferon-induced gene transcription.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

View Samples
accession-icon SRP188096
Transcription profile analysis of wild type and Irf9-/- mouse embryonic fibroblasts (MEF) in response to type I interferons
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Host defense by the innate immune system requires the establishment of antimicrobial states allowing cells to cope with microorganisms before the onset of the adaptive immune response. Interferons (IFN) are of vital importance in the establishment of cell-autonomous antimicrobial immunity. Speed is therefore an important attribute of the cellular response to IFN. With much of the antimicrobial response being installed de novo, this pertains foremost to gene expression, the rapid switch between resting-state and active-state transcription of host defense genes. Our results show how mRNA expression changes upon IFNb treatment in wild type and Irf9-/- mouse embryonic fibroblasts. Overall design: Methods: Mouse embryonic fibroblast (MEF) mRNA of wild-type (WT) and Irf9 knock out mice (IRF9-/-) untreated, as well as 2h IFNb treated were generated by deep sequencing, in triplicate, using Illumina sequencing.

Publication Title

A molecular switch from STAT2-IRF9 to ISGF3 underlies interferon-induced gene transcription.

Sample Metadata Fields

Subject

View Samples
accession-icon SRP188099
Transcription profile analysis of wild type and Irf9-/- human monocytic THP1 cells in response to type I interferons
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Host defense by the innate immune system requires the establishment of antimicrobial states allowing cells to cope with microorganisms before the onset of the adaptive immune response. Interferons (IFN) are of vital importance in the establishment of cell-autonomous antimicrobial immunity. Speed is therefore an important attribute of the cellular response to IFN. With much of the antimicrobial response being installed de novo, this pertains foremost to gene expression, the rapid switch between resting-state and active-state transcription of host defense genes. Our results show how mRNA expression changes upon IFNb treatment in wild type and Irf9-/- THP1 cells. Overall design: Methods: mRNA of untreated and IFNb treated wild-type (WT) and Irf9 knock out (IRF9-/-) human monocytic THP1 cells were analyzed by deep sequencing, in triplicate, using Illumina sequencing.

Publication Title

A molecular switch from STAT2-IRF9 to ISGF3 underlies interferon-induced gene transcription.

Sample Metadata Fields

Subject

View Samples
accession-icon SRP087634
Transcriptome analysis of Listeria monocytogenes infected bone marrow derived macrophages with or without DEAD-box helicase DDX3X
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Bone marrow derived macrophages were infected with Listeria monocytogenes for 4 hours. We investigated differently expressed genes in the absence of DDX3X upon infection and also in steady state conditions. Overall design: Investigation of gene expression in wt and Ddx3x deficient bone marrow derived macrophages in response to Listeria monocytogenes infection.

Publication Title

The RNA helicase DDX3X is an essential mediator of innate antimicrobial immunity.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon GSE97350
ZBTB18 is a repressor of mesenchymal genes in Glioblastoma
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Epigenetic Regulation of ZBTB18 Promotes Glioblastoma Progression.

Sample Metadata Fields

Cell line

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accession-icon GSE97349
ZBTB18 is a repressor of mesenchymal genes in Glioblastoma [JX6]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

The transcriptional repressor ZBTB18 was overexpressed in the brain tumor xenoline JX6 by lentiviral transduction. Three independent transduction were performed (biological replicates) and analyzed by gene expression aray. Gene set enrichemnt analysis (GSEA) showed changes in the expression of mesenchymal signature. A subset of genes was further valiadted by qPCR. These results indicate a role of ZBTB18 as repressor of mesenchymal genes in Glioblastoma.

Publication Title

Epigenetic Regulation of ZBTB18 Promotes Glioblastoma Progression.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE97347
ZBTB18 is a repressor of mesenchymal genes in Glioblastoma [BTSC233]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

The transcriptional repressor ZBTB18 was overexpressed in the brain tumor stem cell-like BTSC233 by lentiviral transduction. Three independent transduction were performed (biological replicates) and analyzed by gene expression aray. Gene set enrichemnt analysis (GSEA) showed changes in the expression of mesenchymal signature. A subset of genes was further valiadted by qPCR. These results indicate a role of ZBTB18 as repressor of mesenchymal genes in Glioblastoma.

Publication Title

Epigenetic Regulation of ZBTB18 Promotes Glioblastoma Progression.

Sample Metadata Fields

Cell line

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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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