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GSE15741
Mus musculus
6 Downloadable Samples
Description
Metastatic disease is a primary cause of cancer-related death, and factors governing tumor cell metastasis have not been fully elucidated. Here we addressed this question by using tumor cell lines derived from mice that develop metastatic lung adenocarcinoma owing to expression of mutant K-ras and p53. A feature of metastasis-prone tumor cells that distinguished them from metastasis-incompetent tumor cells was plasticity in response to changes in their microenvironment. They transited reversibly between epithelial and mesenchymal states, forming highly polarized epithelial spheres in 3-dimensional culture that underwent epithelial-mesenchymal transition (EMT) following treatment with transforming growth factor-beta or injection into syngeneic mice. This plasticity was entirely dependent upon the microRNA-200 family, which decreased during EMT. Forced expression of miR-200 abrogated the capacity of these tumor cells to undergo EMT, invade, and metastasize and conferred transcriptional features of metastasis-incompetent tumor cells. We conclude that microenvironmental cues direct tumor metastasis by regulating miR-200 expression.
Publication Title
Contextual extracellular cues promote tumor cell EMT and metastasis by regulating miR-200 family expression.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 24 Downloadable Samples
Description
Huntington's disease (HD) features a unique disease-initiating mechanism hypothesized to entail an impact of the CAG repeat encoded polyglutamine region on the full-length huntingtin protein, with dominant effects that are continuous with CAG size, in a simple gain of function. To evaluate these predictions, we generated a series of heterozygous Hdh CAG knock-in mouse embryonic stem (ES) cell lines, with 18, 48, 89, 109 CAGs, and found that a continuous analytic strategy efficiently identified, from genome-wide datasets, 73 genes and 172 pathways whose expression varied continuously with CAG length. The CAG-correlated genes were distinct from the set of 754 genes that distinguished huntingtin null ES cells from wild-type controls, and CAG-correlated pathways did not display a one-to-one correspondence with the 238 pathways altered in huntingtin null ES cells. Rather, the genes that varied with CAG size were either members of the same pathways as altered genes in huntingtin null cells or were members of unique pathways related to these pathways. These findings falsified a gain of function/loss of function proposal but were consistent with the simple gain of novel function mechanism hypothesis. The dominant CAG correlated gene expression changes conformed to the genetic features of the HD initiating mechanism and were system-wide and inter-related with pathways perturbed by lack of full-length huntingtin function, urging system-wide approaches for the discovery and validation of potential modulating factors, in the search for effective HD therapeutics.
Publication Title
HD CAG-correlated gene expression changes support a simple dominant gain of function.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 6 Downloadable Samples
Description
Tumor cells that give rise to metastatic disease are a primary cause of cancer-related death and have not been fully elucidated in patients with lung cancer. Here, we addressed this question by using tissues from a mouse that develops metastatic lung adenocarcinoma owing to expression of mutant K-ras and p53. We identified a metastasis-prone population of tumor cells that differed from those with low metastatic capacity on the basis of having sphere-forming capacity in Matrigel cultures, increased expression of CD133 and Notch ligands, and relatively low tumorigenicity in syngeneic mice. Knockdown of jagged1 or pharmacologic inhibition of its downstream mediator phosphatidylinositol 3-kinase abrogated the metastatic but not the tumorigenic activity of these cells. We conclude from these studies on a mouse model of lung adenocarcinoma that CD133 and Notch ligands mark a population of metastasis-prone tumor cells and that the efficacy of Notch inhibitors in metastasis prevention should be explored.
Publication Title
The Notch ligand Jagged2 promotes lung adenocarcinoma metastasis through a miR-200-dependent pathway in mice.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 25 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
X chromosome control of meiotic chromosome synapsis in mouse inter-subspecific hybrids.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
Description
Noroviruses have been widely recognized for their importance as causative agents of non-bacterial gastroenteritis. Mouse norovirus is the only representative of the norovirus genus, family Caliciviridae, able to grow in cell culture. The aim of this study is to describe the differences in the expression profiles of MNV-1 and mock-infected macrophages (RAW 264.7 cells), in order to better understand the response of the host cell to norovirus infection.
Publication Title
Apoptosis in murine norovirus-infected RAW264.7 cells is associated with downregulation of survivin.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Identification of the cortical neurons that mediate antidepressant responses.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 23 Downloadable Samples
Description
NOD mice are an inbred strain that display enhanced MZ B cell differentiation from an early age. Interestingly, several lines of evidence implicate MZ B cells in this strain as important contributors to the T cell mediated beta cell destruction associated with the development of type 1 diabetes (T1D). In order to develop a better understanding of the underlying causes for augmented MZ B cell production in NOD mice, we obtained the transcriptional profiles of FO and MZ subsets and TR precursors from NOD mice and compared them to those of the B6 strain.
Publication Title
Intrinsic molecular factors cause aberrant expansion of the splenic marginal zone B cell population in nonobese diabetic mice.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
Description
Our laboratory wanted to define the transcription profile of aged skeletal muscle. For this reason, we performed a triplicate microarray study on young (3 weeks) and aged (24 months) gatrocnemius muscle from wild-type C57B16 Mice
Publication Title
Transcriptional profiling of skeletal muscle reveals factors that are necessary to maintain satellite cell integrity during ageing.
Sample Metadata Fields
Sex
View Samples- Mus musculus
- 71 Downloadable Samples
Description
Goal of the experiment: Analysis of gene expression changes in the cortex, striatum, hippocampus, hypothalamus, Drd2-MSNs and Drd1-MSNs of mice with a postnatal, neuron-specific ablation of GLP or G9a as compared to control mice.
Publication Title
Control of cognition and adaptive behavior by the GLP/G9a epigenetic suppressor complex.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 42 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Activity-dependent regulation of inhibitory synapse development by Npas4.
Sample Metadata Fields
No sample metadata fields
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