Abhd15 is mainly expressed in white adipose tissues and highly upregulated upon adipogenesis. Abhd15 expression is correlated with insulin resistance in obese humans, however its physiological function remains unknown. We used the microarray technology to gain insight into ABHD15s physiological function by identifying dysregulated genes in eWAT from Abhd15-ko mice in comparison to WT mice.
Loss of ABHD15 Impairs the Anti-lipolytic Action of Insulin by Altering PDE3B Stability and Contributes to Insulin Resistance.
Sex, Specimen part
View SamplesKlotho is critical for the survival of triple negative breast cancer (TNBC) cells HCC1395, since its depletion leads to decreased cell viability, cell cycle arrest and apoptosis.
γKlotho is a novel marker and cell survival factor in a subset of triple negative breast cancers.
Specimen part, Cell line
View SamplesPrecise 5' splice site recognition is essential for both constitutive and regulated pre-mRNA splicing. The U1 snRNP specific protein U1C is involved in this first step of spliceosome assembly and important for stabilizing early splicing complexes. We used an embryonically lethal U1C knockout mutant zebrafish, hi1371, to investigate the potential genomewide role of U1C for splicing regulation. Surprisingly, genomewide RNA-Seq analysis of mutant versus wildtype embryos revealed a large set of specific target genes that changed their alternative splicing patterns in the absence of U1C. In sum, our findings provide evidence for a new role of a general snRNP protein, U1C, as a mediator of alternative splicing regulation.
RNA-Seq analysis in mutant zebrafish reveals role of U1C protein in alternative splicing regulation.
No sample metadata fields
View SamplesWe performed genome-wide methylation analysis of primary feto-placental arterial and venous endothelial cells from healthy (AEC and VEC) and GDM complicated pregnancies (dAEC and dVEC). Parallel transcriptome analysis identified variation in gene expression linked to GDM-associated DNA methylation, implying a direct functional link. Pathway analysis found that genes altered by exposure to GDM clustered to functions associated with Cell Morphology and Cellular Movement in both AEC and VEC. Further functional analysis demonstrated that GDM exposed cells have altered actin organization and barrier function.
Human fetoplacental arterial and venous endothelial cells are differentially programmed by gestational diabetes mellitus, resulting in cell-specific barrier function changes.
Specimen part
View SamplesAs susceptibility to many adult disorders originates in utero, we here hypothesized that fetal sex influences gene expression in placental cells and produces functional differences in human placentas. We found that fetal sex differentially affects gene expression in a cell-phenotype dependent manner among all four placental cell-phenotypes studied: cytotrophoblasts, syncytiotrophoblasts, arterial endothelial cells and venous endothelial cells. The markedly enriched pathways in males were identified to be signaling pathways for graft-versus-host disease as well as the immune and inflammatory systems, both supporting the hypothesis that there is reduced maternal-fetal compatibility for male fetuses.
The human placental sexome differs between trophoblast epithelium and villous vessel endothelium.
Sex, Specimen part
View SamplesHypoxia triggers aggressive cancer growth and contributes to chemotherapy resistance. Novel therapeutic strategies aim at targeting hypoxia activated signaling pathways. Tumor hypoxia not only affects neoplastic tumor cells but also the surrounding stroma cells. Therefore, a novel ex vivo model was established, which allows the study of hypoxia effects in fragments of non-small cell lung cancer (NSCLC) with preserved tumor microenvironment and 3D-structure. Microarray analysis identified 107 significantly regulated genes with at least two-fold expression change in hypoxic compared to normoxic fragments. However, only four genes were significantly regulated in both subtypes, adenocarcinoma and squamous cell carcinoma. The hypoxic regulation of these four genes was verified in an independent set using quantitative PCR.
Hypoxia increases membrane metallo-endopeptidase expression in a novel lung cancer ex vivo model - role of tumor stroma cells.
Specimen part, Treatment
View SamplesHuman testicular cells were isolated mechanically and enzymatically from testis of braindead donors and from urological samples. The expression of genes was studied at baseline and 1,25(OH)2D treated conditions.
Testicular synthesis and vitamin D action.
Specimen part
View SamplesWe assessed the response of primary cultures of human trophoblasts to bioactive 1,25 (OH)2D3 and used whole genome microarray to identify innovative hypotheses.
No associated publication
Specimen part, Treatment
View SamplesBackground: Non-coding RNAs and especially microRNAs have been discovered as master regulators of cancer initiation and progression. The aim of our study was to discover and characterize the function of yet uncharacterized microRNAs in human breast carcinogenesis. Methods: In an unbiased approach, we made use of a commonly used model system for breast cancer (BC) stem cells (mammospheres) to identify whole miRNome alterations with a special focus on previously uncharacterized miRNAs in BC. We further characterized the influence of microRNA-1287-5p, a yet uncharacterized microRNA in BC, in patient samples (n=1262) and on several hallmarks of cancer in vitro and in vivo with a special focus on triple negative BC. The molecular mode of action was further characterized using whole transcriptome analysis, in silico prediction tools, miRNA-interaction luciferase assays and pheno-copy assays. Results: We identified miR-1287-5p among many others as differentially expressed in mammospheres. Clinical validation indicated that miR-1287-5p is significantly downregulated in human BC and associated with poor prognosis. This clinical finding can be explained by miR-1287-5p mediated growth inhibitory effects, G1 cell cycle arrest, decreased anchorage-independent growth and tumor growth in vivo. Finally, we identified PIK3CB as a direct molecular interactor of miR-1287-5p and a pheno-copy factor for miR-1287-5p. Finally, targeting PI3K-signaling pathway with chemical inhibitors together with miR-1287-5p mimics increased the pharmacological growth inhibitory potential. Conclusion: In conclusion, our data identified for the first time an involvement of miR-1287-5p in human BC and suggest a potential for therapeutic interventions in hardly to treat triple negative BC.
No associated publication
Cell line
View SamplesMicroarray profiling was used to determine the most abundantly expressed genes in spinophilin-silenced breast cancer cells compared to control cells in the cell line SUM159. We identified several differentially expressed genes in spinophilin-silenced cells.
No associated publication
Cell line
View Samples