We use single-cell RNA sequencing (scRNA-seq) to explore the transcriptional changes associated with estrogen-induced dysplasia in mouse ovarian surface epithelial cells Overall design: scRNA-seq of control and estrogen-treated (100nM) mOSE cultured for 15 days. scRNA-seq was performed using the Fluidigm HT 3' RNA-seq protocol on the Fluidigm C1
Single-cell RNA-sequencing reveals transcriptional dynamics of estrogen-induced dysplasia in the ovarian surface epithelium.
Specimen part, Treatment, Subject
View SamplesWe used microarray analysis to profile the function of TCF7L1 in human embryonic stem cells.
TCF7L1 suppresses primitive streak gene expression to support human embryonic stem cell pluripotency.
Cell line
View SamplesWe used microarray analysis to profile the function of TCF7L1 in human embryonic stem cells.
TCF7L1 suppresses primitive streak gene expression to support human embryonic stem cell pluripotency.
Specimen part, Cell line
View SamplesHuman tumours show a high level of clonal heterogeneity that contributes to malignant progression and metastasis, but the processes that influence the timing of metastatic dissemination of subclones are unknown. Here, we have used whole exome sequencing of 98 matched benign, malignant, and metastatic skin tumours from genetically heterogeneous mice to demonstrate that most metastases disseminate synchronously from the primary tumour, but then evolve separately, acquiring an additional set of mutations during growth at distant sites. Shared mutations between primary carcinomas and their matched metastases have the distinct A>T signature of the initiating carcinogen Dimethylbanzanthracene (DMBA), but non-shared mutations are primarily G>T or C>T substitutions, associated with oxidative stress. We found recurrent point mutations in several hundred genes, including several in the Ras (Hras, Kras, and Pik3ca) pathway. We propose that carcinogen-driven mouse tumour models can aid our understanding of the forces that shape clonal and genetic evolution of human cancers.
Evolution of metastasis revealed by mutational landscapes of chemically induced skin cancers.
Sex
View SamplesG9a mediates a transcriptional switch, and activates the Notch pathway to coordinate endothelial cell and trophoblast proliferation to promote vascular maturation in the placenta. Overall design: Examination of global transcriptional profiles in control and mutant placenta labyrinth at 2 developmental stages (E12.5 and 13.5).
G9a controls placental vascular maturation by activating the Notch Pathway.
Specimen part, Subject
View SamplesPurpose: Aim of the study is to identify functional differences between the P1 and P2-HNF4a isoforms. To do this, we generated Tet-On inducible lines that express either the human (P1) HNF4a2 or (P2) HNF4a8 under control of DOX in the HCT116 human colon cancer cells. Methods: HNF4a2 and Parental lines were induced with 0.3 µg/mL DOX, while HNF4a8 line was induced with either 0.1 or 0.3 µg/mL DOX for 24 hours. Samples were generated by deep sequencing, using the Illumina TruSeq RNA. Result: There were common and unique dysregulated genes identified in the HNF4a2 and HNF4a8 lines (+DOX); more upregulated genes than downregulated genes in both the lines. Conclusion: The functional difference between HNF4a2 and HNF4a8 is that the latter tends to upregulate genes involved in proliferation and anti-apoptosis while HNF4a2 upregulates genes involved in growth suppression and cell death. Overall design: Tet-On inducible HCT116 cell (Parental, HNF4a2, and HNF4a8) lines, treated with (0.0, 0.1, or 0.3 µg/mL) DOX for 24 hours, were 50bp pair-ended sequenced in triplicate using Illumina TruSeq RNA Sample Prep v2 Kit.
Differential Effects of Hepatocyte Nuclear Factor 4α Isoforms on Tumor Growth and T-Cell Factor 4/AP-1 Interactions in Human Colorectal Cancer Cells.
No sample metadata fields
View SamplesAutophagy is a starvation response that facilitates cell survival under metabolic stress and yet defects in autophagy promote tumorigenesis. While the role of understarvation is relatively clearer, its mechanistic role in tumorigenesis is poorly understood. We show that defective autophagy promotes protein damage and accumulation of p62, a marker for protein damage accumulation that is cleared through autophagy pathway. The failure to eliminate p62 in autophagy-defective cells, leads to deregulation of cell signalling and gene expression and ultimately promotes tumorigenesis. Thus defective-autophagy is a mechanism for p62 accumulation commonly observed in human tumors.
Autophagy suppresses tumorigenesis through elimination of p62.
Cell line
View SamplesWe examined the effect of ablation of Tet2, an epigenetic regulator of gene transcription, in the global programme of gene expression at baseline, without pro-inflammatory activation, in macrophages.
Clonal hematopoiesis associated with TET2 deficiency accelerates atherosclerosis development in mice.
No sample metadata fields
View SamplesWe examined the effect of ablation of Tet2, an epigenetic regulator of gene transcription, in the global programme of gene expression underlying pro-inflammatory activation of macrophage.
Clonal hematopoiesis associated with TET2 deficiency accelerates atherosclerosis development in mice.
Specimen part
View SamplesTransforming growth factor beta 1 (TGF-1) is the most extensively studied growth factor in dentin-pulp complex, with pleiotropic effects on pulp response and healing. Our main objective was to analyze the expression profile of pulp tissue and odontoblasts, and the effects of TGF-1 on these profiles in cultured human pulp and odontoblasts with a specific interest in the anti- and pro-inflammatory cytokines.
Effects of TGF-beta 1 on interleukin profile of human dental pulp and odontoblasts.
No sample metadata fields
View Samples