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GSE23641
Mus musculus
2 Downloadable Samples
Description
We used microarrays to look at overall gene expression differences between miR-155-/- and WT dendritic cells under inflammatory conditions.
Publication Title
MicroRNA-155 promotes autoimmune inflammation by enhancing inflammatory T cell development.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 64 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
A mouse model of the most aggressive subgroup of human medulloblastoma.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 64 Downloadable Samples
Description
Mouse models of medulloblastoma are compared to human subgroups through microarray expression and other measures
Publication Title
A mouse model of the most aggressive subgroup of human medulloblastoma.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 5 Downloadable Samples
Description
To elucidate the mechanisms by which the mir-200 and the miR-183~96~182 cluster could regulate EMT and thus cellular migration, invasion and metastasis in NSCLC, we searched for common predicted targets of these microRNA families that might have a potential role in these biological processes. First we performed a cross comparison of multiple gene expression datasets from our mouse models of metastasis. We overlapped 224 genes that were elevated greater than four-folds upon Zeb1 induction in 393P cells with 210 genes that showed greater than two-fold increase in expression in the metastatic 344SQ cells compared to the non-metastatic 393P cells and 143 genes that were repressed to less than 0.5-fold in cells with exogenous expression of miR-200. This resulted in an enriched list of 45 genes that are potential miR-200 targets having a role in the process of EMT and metastasis. Next we performed an overlap of genes that were predicted targets of the miR-200 family members and the miR-183~96~182 cluster using the microRNA prediction algorithms miRanda (www.microRNA.org) and identified a list of 17 highly conserved common targets with a mirSVR score less than -6.0. The only 2 genes common in both the overlapping subsets were Zeb1 and Foxf2.
Publication Title
The miR-200 family and the miR-183~96~182 cluster target Foxf2 to inhibit invasion and metastasis in lung cancers.
Sample Metadata Fields
Cell line, Treatment
View Samples- 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
- 27 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Expression signatures of metastatic capacity in a genetic mouse model of lung adenocarcinoma.
Sample Metadata Fields
No sample metadata fields
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
- 8 Downloadable Samples
Description
Diet-induced obesity (DIO) is rapidly becoming a global health problem, particularly as Westernization of emerging nations continues. Currently, one third of adult Americans are considered obese and, if current trends continue, >90% of US citizens are predicted to be affected by 2050. However, efforts to fight this epidemic have not yet produced sound solutions for prevention or treatment. Our studies reveal a balanced and chronobiological relationship between food consumption, daily variation in gut microbial evenness and function, basomedial hypothalamic circadian clock (CC) gene expression, and key hepatic metabolic regulatory networks , including CC and nuclear receptors (NR), that is are essential for metabolic homeostasis. Western diets high in saturated fats dramatically alter diurnal variation in microbial composition and function, which in turn lead to uncoupling of the hepatic CC and NR networks from central CC control in ways that offset the timing and types of regulatory factors directing metabolic function. These signals include microbial metabolites such as short chain fatty acids (SCFAs) and hydrogen sulfide (H2S) that can directly regulate or disrupt metabolic networks of the hepatocyte. Our study therefore provides insights into the complex and dynamic relationships between diet, gut microbes, and the host that are critical for maintenance of health. Perturbations of this constellation of processes, in this case by diet-induced dysbiosis and its metabolomic signaling, can potentially promote metabolic imbalances and disease. This knowledge opens up many possibilities for novel therapeutic and interventional strategies to treat and prevent DIO, ranging from the manipulation of gut microbial function to pharmacological targeting of host pathways to restore metabolic balance.
Publication Title
Effects of diurnal variation of gut microbes and high-fat feeding on host circadian clock function and metabolism.
Sample Metadata Fields
Specimen part
View Samples