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GSE36111
Homo sapiens
5 Downloadable Samples
Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
A cancer stem cell cannot be identified solely based on surface markers as none of the markers used to isolate stem cells in various normal and cancerous tissues is expressed exclusively by stem cells. Our experimental results have also identified additional fractions representing true stem-like cells in oral squamous cell carcinoma (OSCC), refuting the concept that cancer stem cells (CSCs) are a rare population, and we have also developed an in vitro model to explore the stem cell concept in oral epithelial tumorigenesis. This model expounds four distinct fractions within a homogenous cell line SCC172 that is morphologically similar (85% cells expressing CSC markers), yet varying in all functional aspects of cell cycle, dye retention, chemoresistance, tumor-forming potential, self renewal, apoptosis resistance and regulation at molecular levels. Relating to our CSC shift model, we analysed the concept of biological heterogeneity in terms of four fractions SP1, SP2, MP1 and MP2 and associated it with variations among patients in a clinical scenario.
Publication Title
Analysis of MicroRNA-mRNA Interactions in Stem Cell-Enriched Fraction of Oral Squamous Cell Carcinoma.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 3 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
We have analyzed the effects of IL-21 signaling on T cell activation, IL-22 production and gut inflammation
Publication Title
IL-21 induces IL-22 production in CD4+ T cells.
Sample Metadata Fields
Age, Specimen part, Treatment
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
During late gestation, structures called villi extend into the intestinal lumen to dramatically increase the surface area of the intestinal epithelium, preparing the gut for the neonatal diet. Incomplete development of the intestine is the most common gastrointestinal complication in neonates, but the causes are unclear. We provide evidence that Yin-Yang1 (Yy1) is critical for intestinal villus development. YY1 loss in the developing endoderm had no apparent consequences until late gestation, after which the intestine differentiated poorly and exhibited severely stunted villi. Transcriptome analysis revealed that YY1 is required for mitochondrial gene expression, and ultrastructural analysis confirmed compromised mitochondrial integrity in the mutant intestine. We found increased oxidative phosphorylation gene expression at the onset of villus elongation, suggesting that aerobic respiration may function as a regulator of villus growth. Mitochondrial inhibitors blocked villus growth in a fashion similar to Yy1 loss, thus further linking oxidative phosphorylation with late-gestation intestinal development. Interestingly, we find necrotizing enterocolitis patients also exhibit decreased expression of oxidative phosphorylation genes. Our study highlights the still unappreciated role of metabolic regulation during organogenesis, and suggests it may contribute to neonatal gastrointestinal disorders.
Publication Title
A YY1-dependent increase in aerobic metabolism is indispensable for intestinal organogenesis.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 16 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Since the initial discovery that OCT4, SOX2, KLF4 and c-MYC overexpression sufficed for the induction of pluripotency in somatic cells, methodologies replacing the original factors have enhanced our understanding of the reprogramming process. However, unlike in mouse, OCT4 has not been replaced successfully during reprogramming of human cells. Here we report on a strategy to do so. Through a combination of transcriptome and bioinformatic analysis we have identified factors previously characterized as being lineage specifiers that are able to replace OCT4 and SOX2 in the reprogramming of human fibroblasts. Our results show that is possible to replace OCT4 and SOX2 simultaneously with alternative lineage specifiers in the reprogramming of human cells. At a broader level, they also support a model in which counteracting lineage specification networks underlie the induction of pluripotency,
Publication Title
Reprogramming of human fibroblasts to pluripotency with lineage specifiers.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 189 Downloadable Samples
Illumina HiSeq 3000
Description
The weekly turnover of the intestinal epithelium is driven by multipotent, Lgr5+, crypt base columnar cells (CBCs). In response to injury, however, Lgr5+ cells are lost but then re-emerge and are required for successful recovery. How these resurgent Lgr5+ stem cells arise is unclear. We transcriptionally profiled single cells from regenerating intestinal epithelia and identified a unique cell type we term the revival stem cell (rSC). rSCs are mutually exclusive to CBCs and are distinguished by elevated expression of cell survival and DNA repair genes. In homeostasis, rSCs are extremely rare, but nevertheless give rise to all the major cell types of the intestine including crypt-villus axes. After damage rSCs display a 20-fold, Yap-dependent, transient expansion, reconstitute the Lgr5+ CBC compartment and are required to regenerate a functional intestine. These studies define a unique stem cell phenotype that is mobilized by damage to reconstitute the intestinal epithelium. Overall design: Examination of regenerating mouse intestinal epithelium.
Publication Title
Single-cell transcriptomes of the regenerating intestine reveal a revival stem cell.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Homo sapiens
- 11 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Tumors consist of heterogeneous cell population, containing cancer cell subpopulations with anticancer drug-resistant property, called “persister” cells. To reveal the character of the persister cells, we analyzed gene expression profile of patient-derived gastric cells and residual cancer cells after treatment with 5-FU or SN38, an active metabolite of irinotecan. In our study, we identified ALDH1A3 as a marker and a cell proliferation factor of persister cells. To examine molecular pathways regulated by ALDH1A3, we analyzed gene expression profile of patient-derived gastric JSC15-3 in which ALDH1A3 was knocked down by using shRNAs.
Publication Title
ALDH1A3-mTOR axis as a therapeutic target for anticancer drug-tolerant persister cells in gastric cancer.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Mus musculus
- 16 Downloadable Samples
- Illumina HiSeq 2000
Description
Maintenance of vascular integrity in the adult animal is needed for survival and critically dependent on the endothelial lining, which controls barrier function, blood fluidity, and flow dynamics. However, nodal regulators that coordinate endothelial identity and function in the adult animal remain poorly characterized. Here we show that endothelial KLF2 and KLF4 control a large segment of the endothelial transcriptome thereby affecting virtually all key endothelial functions. Inducible endothelial-specific deletion of Klf2 and/or Klf4 reveals that a single allele of either gene is sufficient for survival, but absence of both (EC-DKO) results in acute death from myocardial infarction, heart failure, and stroke. EC-DKO animals exhibit profound compromise in vascular integrity and profound dysregulation of the coagulation system. Collectively, these studies establish an absolute requirement for KLF2/4 for maintenance of endothelial and vascular integrity in the adult animal. Overall design: Eight-to-ten-week old mice were intraperitoneally injected with tamoxifen to trigger endothelial-specific gene deletion of KLF2 and/or KLF4. At day 6 post-injection, endothelial cells were isolated from the heart and total RNA was purified.
Publication Title
KLF2 and KLF4 control endothelial identity and vascular integrity.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Gene expression from iPSCs before and after gene correction
Publication Title
Targeted gene correction of laminopathy-associated LMNA mutations in patient-specific iPSCs.
Sample Metadata Fields
Specimen part
View Samples- Rattus norvegicus
- 2 Downloadable Samples
- Illumina HiSeq 2500
Description
Heart failure is a leading cause of mortality and morbidity in the developed world, partly because mammals lack the ability to regenerate heart tissue. Whether this is due to evolutionary loss of regenerative mechanisms present in other organisms or to an inability to activate such mechanisms is currently unclear. Here, we decipher mechanisms underlying heart regeneration in adult zebrafish and show that the molecular regulators of this response are conserved in mammals. We identified miR-99/100 and Let-7a/c, and their protein targets smarca5 and fntb, as critical regulators of cardiomyocyte dedifferentiation and heart regeneration in zebrafish. Although human and murine adult cardiomyocytes fail to elicit an endogenous regenerative response following myocardial infarction, we show that in vivo manipulation of this molecular machinery in mice results in cardiomyocyte dedifferentiation and improved heart functionality after injury. These data provide a proof-of-concept for identifying and activating conserved molecular programs to regenerate the damaged heart. Overall design: RNA-Seq expression profiles of rat cardiomyocytes after knockdown of miR-99/100 and Let-7 miRNAs
Publication Title
In vivo activation of a conserved microRNA program induces mammalian heart regeneration.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 15 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
In neural stem cells, stimulation of the death receptor CD95 does not trigger apoptosis but resulted in increased stem cell survival and neuronal specification via activation of the Src /PI3K /AKT/mTOR signalling pathway. To further characterize CD95-dependent neural stem cell survival and differentiation we used conventional gene expression profiling combined with translation state array analysis. Mouse neural stem cells grown in neurosphere cultures were stimulated with a trimerized CD95L construct (CD95L-T4) and total as well as polysomal bound RNA was isolated 48 hours after stimulation and analysed by microarrays. CD95L-T4 treatment induced a global increase in ribosome-bound mRNA and protein translation as well as changes on genes involved in neurogenesis, protein synthesis and transcription factors.
Publication Title
The death receptor CD95 activates adult neural stem cells for working memory formation and brain repair.
Sample Metadata Fields
Sex, Treatment
View Samples