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accession-icon GSE71242
Gene dosage imbalance contributes to chromosomal instability-induced tumorigenesis
  • organism-icon Drosophila melanogaster
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Chromosomal instability (CIN) is thought to be a source of mutability in human cancer. However, CIN is highly deleterious for the cell, and the resulting aneuploidy induces metabolic stress and compromises cell fitness. Here we utilized the X-chromosome dosage compensation mechanism and changes in X-chromosome number to demonstrate in Drosophila epithelial cells the causal relationship between CIN, aneuploidy, gene dosage imbalance and tumorigenesis. Whereas the harmful effects of CIN can be buffered by resetting the X-chromosome dosage compensation to compensate for changes in X-chromosome number, interfering with the mechanisms of dosage compensation suffices to induce tumorigenesis. In addition, multiple mechanisms buffer the deleterious effects of CIN including DNA-damage repair, activation of the p38 signalling pathway, and induction of cytokine expression to promote compensatory cell proliferation. These data reveal a key role of gene dosage imbalances to CIN-induced programmed cell death and tumorigenesis and the existence of robust compensatory mechanisms.

Publication Title

Gene Dosage Imbalance Contributes to Chromosomal Instability-Induced Tumorigenesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE38088
Expression data from human induced pluripotent stem cell-derived teratomas and embryoid bodies
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The tumorigenicity of human pluripotent stem cells (hPSCs) is a major safety concern for their application in regenerative medicine. Here we identify the tight-junction protein Claudin-6 as a specific cell surface marker of hPSCs that can be used to selectively remove Claudin-6-positive cells from mixed cultures. We show that Claudin-6 is absent in adult tissues but highly expressed in undifferentiated cells, where it is dispensable for hPSC survival and self-renewal. We use three different strategies to remove Claudin-6-positive cells from mixed populations: an antibody against Claudin-6; a cytotoxin-conjugated antibody that selectively targets undifferentiated cells; and clostridium perfringens enterotoxin, a toxin that binds several Claudins, including Claudin-6, and efficiently kills undifferentiated cells, thus eliminating the tumorigenic potential of hPSC-containing cultures. This work provides a proof of concept for the use of Claudin-6 to eliminate residual undifferentiated hPSCs from culture, highlighting a strategy that may increase the safety of hPSC-based cell therapies.

Publication Title

Immunologic and chemical targeting of the tight-junction protein Claudin-6 eliminates tumorigenic human pluripotent stem cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE33710
Transcriptomic datat of senescence WI-38 cell
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Senescence in WI-38 cell context was induce by RASv12 over expression Cellular senescence is a permanent cell cycle arrest that is triggered by cancer- initiating or promoting events in mammalian cells and is now considered a major tumour suppressor mechanism. Here, we did a transcriptomic analysis and compared WI-38 contol wich is a human fibroblaste cell line and WI-38 that overexpressed RASv12 a G protein that induce senescence. The goal of our project is to compare transciptomic profile of human growing fibroblast (WI-38 control) and senescent human fibroblast (WI-38 OERAS)

Publication Title

Senescence is an endogenous trigger for microRNA-directed transcriptional gene silencing in human cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE57909
Expression data from human pluripotent stem cells treated with PluriSIn#2
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Pluripotent-specific inhibitors (PluriSIns) make a powerful tool for studying the mechanisms that control the survival of human pluripotent stem cells (hPSCs). Here we characterize PluriSIn#2 as a novel selective indirect inhibitor of topoisomerase II alpha (TOP2A). We find that TOP2A is uniquely expressed in undifferentiated hPSCs, and that its inhibition results in their rapid cell death. These findings reveal a dependency of hPSCs on the activity of TOP2A, which can be harnessed for their selective elimination from culture.

Publication Title

Brief reports: Controlling the survival of human pluripotent stem cells by small molecule-based targeting of topoisomerase II alpha.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon SRP009864
High-throughput sequencing of AGO-immunoprecipitating miRs in human senescent fibroblast WI-38
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

In humans, there are four Ago proteins (Ago1–4) and AGO1- and 2 were previously implicated in TGS induced by exogenous siRNAs and microRNAs (miRs) directed against gene promoter transcripts via promotion of changes in histone covalent modifications and DNA methylation. Not-with-standing, many mechanistic details of this process remain poorly defined in human cells, and very little is known about the identity of possible endogenous signals, which may drive this process in human cells. Given the evolutionary conserved role of siRNAs and AGO proteins in TGS and heterochromatin formation, we set out to analyse their possible involvement in senesence-associated repression of E2F target genes. To obtain a detailed picture of AGO-immunoprecipitating miRs (RIP) in senescent cells, we used next-generation sequencing (NGS)(RIP-Seq). We also included histone H3 dimethylated on lysine 9 (H3K9me2) in this analysis to assign potential AGO2-interacting miRs to a repressive chromatin state and unfractionated, cellular RNA from senescent cells for normalisation. Overall design: Determination of AGO AGO-immunoprecipitating miRs in WI-38 senescent human fibroblast

Publication Title

Senescence is an endogenous trigger for microRNA-directed transcriptional gene silencing in human cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE93188
Transcriptomic fingerprints of C. elegans exposed to citrate coated superparamagnetic iron oxide nanoparticles (C-SPIONs) and to superparamagnetic iron oxide nanoparticles coated with a monolayer of bovine serum albumin (BSA-SPIONs)
  • organism-icon Caenorhabditis elegans
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Gene 1.0 ST Array (elegene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Toxicogenomics of iron oxide nanoparticles in the nematode C. elegans.

Sample Metadata Fields

Specimen part

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accession-icon GSE93187
Transcriptomic fingerprints of C. elegans exposed to citrate coated superparamagnetic iron oxide nanoparticles (C-SPIONs)
  • organism-icon Caenorhabditis elegans
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Gene 1.0 ST Array (elegene10st)

Description

Superparamagnetic Iron Oxide Nanoparticles (SPIONs) are currently being investigated for a range of biomedical applications. Their use have been related with different cytotoxic mechanisms including the generation of oxidative stress and the induction of metal detoxification pathways, among others. We have investigated the molecular mechanisms responsive to in-house fabricated citrate coated SPIONs (C-SPIONs) in the nematode C. elegans to compare in vivo findings with previous in vitro studies. C-SPIONs (500 g/ml) affected the transcriptional response of signal transduction cascades (i.e. TFG-beta), protein processing in the endoplasmic reticulum, and RNA transport, among other biological processes. They also triggered a lysosomal response, indicating a relevant biological role of this cellular compartment in the response to this nanoparticle treatment in C. elegans. Interestingly, other pathways frequently linked to nanotoxicity like oxidative stress or apoptosis were not identified as significantly affected in this genome-wide in vivo study despite the high dose of exposure.

Publication Title

Toxicogenomics of iron oxide nanoparticles in the nematode C. elegans.

Sample Metadata Fields

Specimen part

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accession-icon GSE93186
Transcriptomic fingerprints of C. elegans exposed to superparamagnetic iron oxide nanoparticles coated with a monolayer of bovine serum albumin (BSA-SPIONs)
  • organism-icon Caenorhabditis elegans
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Gene 1.0 ST Array (elegene10st)

Description

Superparamagnetic Iron Oxide Nanoparticles (SPIONs) are currently being investigated for a range of biomedical applications. Their use have been related with different cytotoxic mechanisms including the generation of oxidative stress and the induction of metal detoxification pathways, among others. Different NP coatings are being explored, among them albumin which has been applied in some drugs delivery systems. We have investigated the molecular mechanisms responsive to in-house fabricated SPIONs coated with bovine serum albumin (BSA-SPIONs) in the nematode C. elegans to compare in vivo findings with previous in vitro studies. BSA-SPIONs (500 g/ml) affected the transcriptional response of glycan metabolic pathways related to innate immune response, xenobiotics degradation, and triggered a lysosomal response, indicating a relevant biological role of this cellular compartment in the response to this nanoparticle treatment in C. elegans. Remarkably, key biological functions such as apoptosis or protein processing were not affected with significance despite the high dose of exposure.

Publication Title

Toxicogenomics of iron oxide nanoparticles in the nematode C. elegans.

Sample Metadata Fields

Specimen part

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accession-icon GSE19083
Microarray analysis of mediastinal lymph node of pigs naturally affected by postweaning multisystemic wasting syndrome
  • organism-icon Sus scrofa
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Porcine Genome Array (porcine)

Description

Postweaning multisystemic wasting syndrome (PMWS) is one of the pig diseases with major economic impact worldwide. Clinical, pathologic and some immunologic aspects of this disease are well-known, but the molecular mechanisms underlying pathogenic mechanisms of the disease are still poorly understood. The objective of the present study was to investigate the global changes in gene expression in the mediastinal lymph nodes from pigs naturally affected by PMWS and healthy counterparts, using the Affymetrix Porcine Genechip. This is the first study on gene expression in pigs naturally affected by PMWS. The present results allowed identifying potential mechanisms underlying the inflammation, lymphocyte depletion in lymphoid tissues and immune suppression, which are key features of PMWS.

Publication Title

Microarray analysis of mediastinal lymph node of pigs naturally affected by postweaning multisystemic wasting syndrome.

Sample Metadata Fields

Age, Specimen part, Disease, Disease stage

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accession-icon GSE31774
Effect of loss of function of Gal11/Med15 and Med3 from the Mediator tail module in budding yeast
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Gene expression was compared for wild type yeast (BY4741) and yeast lacking Gal11/Med15 and Med3, or from a gal11-myc med3 strain. The gal11-myc allele shows a partial loss of function when combined with med3. Expression was analyzed for yeast grown in YPD as well as in CSM.

Publication Title

Distinct role of Mediator tail module in regulation of SAGA-dependent, TATA-containing genes in yeast.

Sample Metadata Fields

No sample metadata fields

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

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