We show that numerous miRNAs are transcriptionally up-regulated in papillary thyroid carcinoma (PTC) tumors compared with unaffected thyroid tissue. Among the predicted target genes of the three most upregulated miRNAs (miRs 221, 222 and 146b), only less than 15% showed significant downexpression in transcript level between tumor and unaffected tissue. The KIT gene which is known to be downregulated by miRNAs 221 and 222 displayed dramatic loss of transcript and protein in those tumors that had abundant mir-221, mir-222, and mir-146b transcript.
The role of microRNA genes in papillary thyroid carcinoma.
Specimen part
View SamplesDifferential gene expression analysis of parental and sub-lines of melanoma cell line resistant to F5 CTL lymphocyte
Molecular mechanism of MART-1+/A*0201+ human melanoma resistance to specific CTL-killing despite functional tumor-CTL interaction.
Cell line
View SamplesAnalysis of gene expression profile of B16-F10 murine melanoma cells exposed to hypoxic conditions (1% oxygen) or hypoxia mimicry (cobalt chloride) for 24 hours. Gene expression profiles were analyzed using MG-U74Av2 oligonucleotide microarrays. Data analysis revealed 2541 probesets (FDR<5%) for 1% oxygen experiment and 364 probesets (FDR<5%) for cobalt chloride, that showed differences in expression levels. Analysis of hypoxia-regulated genes (1% O2) by stringent Family-Wise Error Rate estimation indicated 454 significantly changed transcripts (p<0.05). The most upregulated genes were Lgals3, Selenbp1, Nppb (more than ten-fold increase). Both hypoxia and hypoxia-mimicry induced HIF-1 regulated genes. However, unsupervised analysis (Singular Value Decomposition) revealed distinct differences between gene expression induced by these two experimental conditions.
Gene expression profile of B 16(F10) murine melanoma cells exposed to hypoxic conditions in vitro.
Cell line
View SamplesA quantitative genetic analysis of the yeast replicative life span was carried out by sampling the natural genetic variation
Natural genetic variation in yeast longevity.
No sample metadata fields
View SamplesFriedreich's ataxia (FRDA) is an autosomal recessive neurodegenerative disease usually caused by large homozygous expansions of GAA repeat sequences in intron 1 of the frataxin (FXN) gene. FRDA patients have low FXN mRNA and frataxin protein levels when compared with heterozygous carriers or healthy controls. Presently, there is no effective treatment for FRDA, and biomarkers to measure therapeutic trial outcomes and/or to gauge disease progression are lacking. Peripheral tissues, including blood cells, buccal cells, and skin fibroblasts, can readily be isolated from FRDA patients and used to define molecular hallmarks of disease pathogenesis. However, because these tissues are not directly involved in disease pathogenesis, their relevance as models of the molecular aspects of the disease is yet to be decided. Transcriptome profiling of FRDA skin fibroblasts revealed significantly upregulated expression of genes encoding plasma membrane solute carrier proteins. Conversely, the expression of genes encoding accessory factors and enzymes involved in cytoplasmic and mitochondrial protein synthesis was consistently decreased in the FRDA cells. Finally, comparison of genes differentially expressed in FRDA fibroblasts to 3 previously published gene expression signatures defined for FRDA blood cells showed substantial overlap between the independent datasets, including correspondingly deficient expression of antioxidant defense genes. Together, these results indicate that gene expression profiling of cells derived from peripheral tissues can, in fact, consistently reveal novel molecular pathways of the disease. Overall design: We used RNA sequencing to profile the transcriptomes of primary fibroblast cell lines derived from 18 FRDA patients and 17 unaffected control individuals.
A Comprehensive Transcriptome Analysis Identifies FXN and BDNF as Novel Targets of miRNAs in Friedreich's Ataxia Patients.
Specimen part, Subject
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