Pulmonary alveoli are complex architectural units thought to undergo endogenous or pharmacologically induced programs of regeneration and degeneration. To study the molecular mechanism of alveoli loss mice were calorie restricted at different timepoints. Lungs were harvested and processed for RNA extraction.
Calorie-related rapid onset of alveolar loss, regeneration, and changes in mouse lung gene expression.
Time
View SamplesIt has been shown that dexamethasone (Dex) impairs the normal lung septation that occurs in the early postnatal period. Treatment with retinoic acid (ATRA) abrogates the effects of Dex. To understand the molecular basis for the Dex indiced inhibition of the formation of the alveoli and the ability of ATRA to prevent the inhibition of septation, gene expression was analyzed in 4-day old mice treated with diluent (control), Dex-treated and ATRA+Dex-treated.
DNA microarray analysis of neonatal mouse lung connects regulation of KDR with dexamethasone-induced inhibition of alveolar formation.
No sample metadata fields
View SamplesForkhead box class O (FoxO) transcription factors regulate whole body energy metabolism, skeletal muscle mass and substrate switching. To elucidate the role of FOXO in skeletal muscle, dominant negative (dn) constructs for FOXO1 (FOXO1dn) or FOXO3 (FOXO3dn) were transfected by electroporation into mouse tibialis anterior muscle and glucose uptake, signal transduction, and glucose stimulated gene expression profiles were assessed. Results were compared against contralateral control transfected muscle.
Regulation of glucose uptake and inflammation markers by FOXO1 and FOXO3 in skeletal muscle.
Sex, Age, Specimen part
View SamplesSalivary tumors isolated from MMTV-ras transgenic mice expressing wild-type p53, no p53 or p53R172H gain-of-funcion mutant were subjected to genome-wide gene expression profiling to assess the effect of the different p53 status on tumor gene expression.
Comparison of effects of p53 null and gain-of-function mutations on salivary tumors in MMTV-Hras transgenic mice.
No sample metadata fields
View SamplesBackground: Turner syndrome, a common sex chromosome aneuploidy, has characteristics and malformations associated with the phenotype. Fetal amniotic fluid is a complex biological material that could contribute to the understanding Turner syndrome pathogenesis. Global gene expression analysis of Turner syndrome fetal amniotic fluid supernatant was utilized to identify organ systems and specific genes that may play a role in the pathophysiologic changes that are seen in individuals with Turner syndrome.
Amniotic fluid RNA gene expression profiling provides insights into the phenotype of Turner syndrome.
No sample metadata fields
View SamplesIdentification of genes that are involved in self-seeding by comparing gene expression profiles between parental MDA-MB-231 cells and seeder cells (MDA-231-S1a and S1b)
Tumor self-seeding by circulating cancer cells.
No sample metadata fields
View SamplesComparisons among breast cancer metastases at different organs revealed distinct microenvironments as characterized by cytokine content.
Latent bone metastasis in breast cancer tied to Src-dependent survival signals.
No sample metadata fields
View SamplesComparisons among breast cancer metastases at different organs revealed distinct microenvironments as characterized by cytokine content.
Latent bone metastasis in breast cancer tied to Src-dependent survival signals.
No sample metadata fields
View SamplesComparisons among breast cancer metastases at different organs revealed distinct microenvironments as characterized by cytokine content.
Latent bone metastasis in breast cancer tied to Src-dependent survival signals.
No sample metadata fields
View SamplesMetastasis-initiating cells dynamically adapt to the distinct microenvironments of different organs, but these early adaptations are poorly understood due to the limited sensitivity of in situ transcriptomics. We developed fluorouracil-labeled RNA sequencing (Flura-seq) for in situ analysis with unprecedented sensitivity. Flura-seq utilizes cytosine deaminase (CD) to convert fluorocytosine to fluorouracil, covalently labeling nascent RNA for purification and sequencing. Flura-seq revealed that breast cancer micrometastases in lung and brain exhibit unique, reversible gene signatures depending on the microenvironment. Specifically, the mitochondrial electron transport Complex I and the NRF2-driven antioxidant programs were induced in oxygen-rich pulmonary micrometastases, compared to mammary tumors or brain micrometastases. Loss of Complex I activity, and antioxidant supplementation potentiated pulmonary metastatic growth. We confirm lung metastasis-specific NRF2 overexpression in clinical samples, thus validating Flura-seq's utility in identifying clinically actionable microenvironmental adaptations in early metastasis. The sensitivity, robustness and economy of Flura-seq are broadly applicable beyond cancer research. Overall design: Examination of 5-FU labeled RNAs in cancer cells present in different organs
Flura-seq identifies organ-specific metabolic adaptations during early metastatic colonization.
Cell line, Subject
View Samples