Genes regulated in different tumor regions, cells isolated by LCM
Estrogen induces c-Kit and an aggressive phenotype in a model of invasive lobular breast cancer.
Specimen part, Treatment
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Chromatinized protein kinase C-θ directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells.
Cell line, Treatment
View SamplesEpithelial to mesenchymal transition (EMT) is activated during cancer invasion and metastasis, enriches for cancer stem cells (CSCs), and contributes to therapeutic resistance and disease recurrence. The epithelial cell line MCF7, can be induced to undergo EMT with the induction of PKC by PMA. 5-10% of the resulting cells have a CSC phenotype. This study looks at the transcriptome of these cells and how it differs from cells with a non-CSC phenotype.
Chromatinized protein kinase C-θ directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells.
Cell line, Treatment
View SamplesVAF347 is a low molecular weight compound which inhibits allergic lung inflammation in vivo. This effect is likely due to a block of dendritic cell (DC) function to generate pro-inflammatory T-helper (Th) cells since VAF347 inhibits IL-6, CD86 and HLA-DR expression by human monocyte derived DC, three relevant molecules for Th-cell generation. Here we demonstrate that VAF347 interacts with the aryl hydrocarbon receptor (AhR) protein resulting in activation of the AhR signaling pathway. Functional AhR is responsible for the biological activity of VAF347 since, i) other AhR agonists display an identical activity profile in vitro, ii) gene silencing of wild type AhR expression or forced over-expression of a trans-dominant negative AhR ablates VAF347 activity to inhibit cytokine induced IL-6 expression in a human monocytic cell line and iii) AhR deficient mice are resistant to the compounds ability to block allergic lung inflammation in vivo. These data identify the AhR protein as key molecular target of VAF347 and its essential role for mediating the anti-inflammatory effects of the compound in vitro and in vivo.
Activation of the aryl hydrocarbon receptor is essential for mediating the anti-inflammatory effects of a novel low-molecular-weight compound.
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CXCL10 is critical for the progression and maintenance of depigmentation in a mouse model of vitiligo.
Specimen part
View SamplesThe transcription factor SRF (serum response factor) mediates epilepsy mediated gene expression
SRF modulates seizure occurrence, activity induced gene transcription and hippocampal circuit reorganization in the mouse pilocarpine epilepsy model.
Specimen part, Treatment
View SamplesSkin samples from mice in a model of vitiligo were selected for gene expression profiling in order to identify active inflammatory pathways.
CXCL10 is critical for the progression and maintenance of depigmentation in a mouse model of vitiligo.
Specimen part
View SamplesThe hormone prolactin is implicated in the pathogenesis of breast cancer, and a subset of prolactin-induced gene expression is mediated by HDAC6 activity.
HDAC6 Deacetylates HMGN2 to Regulate Stat5a Activity and Breast Cancer Growth.
Sex, Specimen part, Cell line
View SamplesMKR mice is a Type 2 Diabetic mice, which was created by expressing mutation in IGF1 receptor in the skeletal muscle, and is widely used in diabetes research. Gene expression differences between MKR mice and Healthy (Wild type) mice are poorly understood.
Multi-tissue computational modeling analyzes pathophysiology of type 2 diabetes in MKR mice.
Age, Specimen part
View SamplesMenopausal estrogen (E2) replacement therapy increases the risk of estrogen receptor (ER)-positive epithelial ovarian cancers (EOC). Whether E2 is tumorigenic or promotes expansion of undiagnosed pre-existing disease is unknown. To determine E2 effects on tumor promotion, we developed an intraperitoneal mouse xenograft model using ZsGreen fluorescent ER- 2008 and ER+ PEO4 human EOC cells. Tumor growth was quantified by in vivo fluorescent imaging. In ER+ tumors, E2 significantly increased size, induced progesterone receptors, and promoted lymph node metastasis, confirming that ER are functional and foster aggressiveness. Laser captured human EOC cells from ER- and ER+ xenografted tumors were profiled for expression of E2-regulated genes. Three classes of E-regulated EOC genes were defined, but less than 10% were shared with E-regulated breast cancer genes. Since breast cancer selective ER modulators (SERM) are therapeutically ineffective in EOC, we suggest that our EOC-specific E-regulated genes can assist pharmacologic discovery of ovarian targeted SERM.
Tissue-specific pathways for estrogen regulation of ovarian cancer growth and metastasis.
Specimen part
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