MiRNAs are essential mediators of many biological processes. The aim of this study was to investigate the dynamics of miRNA-mRNA regulatory networks during exercise and subsequent recovery period.
Dynamically regulated miRNA-mRNA networks revealed by exercise.
Sex, Age
View SamplesAnalysis of differential gene expression for rutured vs stable abdominal aortic aneurysms (AAA) and for intermediate size (55mm) vs large (>70mm) AAA.
Molecular Fingerprint for Terminal Abdominal Aortic Aneurysm Disease.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Adam17 Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling in Mice.
Sex
View SamplesGene expression analysis in tissues of Adam17 hypomorphic and wildtype control C57BL/6 mice.
Adam17 Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling in Mice.
Sex
View SamplesGene expression analysis in tissues of Adam17 hypomorphic and wildtype control C57BL/6 mice.
Adam17 Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling in Mice.
Sex
View SamplesThe loss of E-cadherin causes dysfunction of the cell-cell junction machinery, which is an initial step in epithelial-to-mesenchymal transition (EMT), facilitating cancer cell invasion and the formation of metastases. A set of transcriptional repressors of E-cadherin (CDH1) gene expression, including Snail1, Snail2 and Zeb2 mediate E-cadherin down-regulation in breast cancer. However, the molecular mechanisms underlying the control of E-cadherin expression in breast cancer progression remain largely unknown. Here, by using global gene expression approaches, we uncover a novel function for Cdc42 GTPase-activating protein (CdGAP) in the regulation of expression of genes involved in EMT. We found that CdGAP used its proline-rich domain to form a functional complex with Zeb2 to mediate the repression of E-cadherin expression in ErbB2-transformed breast cancer cells. Conversely, knockdown of CdGAP expression led to a decrease of the transcriptional repressors Snail1 and Zeb2, and this correlated with an increase in E-cadherin levels, restoration of cell-cell junctions, and epithelial-like morphological changes. In vivo, loss of CdGAP in ErbB2-transformed breast cancer cells impaired tumor growth and suppressed metastasis to lungs. Finally, CdGAP was highly expressed in basal-type breast cancer cells, and its strong expression correlated with poor prognosis in breast cancer patients. Together, these data support a previously unknown nuclear function for CdGAP where it cooperates in a GAP-independent manner with transcriptional repressors to function as a critical modulator of breast cancer through repression of E-cadherin transcription. Targeting Zeb2-CdGAP interactions may represent novel therapeutic opportunities for breast cancer treatment. Overall design: Total RNA profiles of ErbB2-expressing control mammary tumor explants cells (shCON) and CdGAP-depleted cells (shCdGAP) were generated by deep sequencing, in triplicate, using Illumina HiSEq2000.
The Cdc42/Rac1 regulator CdGAP is a novel E-cadherin transcriptional co-repressor with Zeb2 in breast cancer.
Specimen part, Subject
View SamplesWe used microarrays to establish whether EBF1 and Pax5 repress similar or unique genes. We found that EBF1 uniquely represses the expression of the T-lineage transcription factor Gata3.
Transcriptional repression of Gata3 is essential for early B cell commitment.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
PGC-1α Promotes Breast Cancer Metastasis and Confers Bioenergetic Flexibility against Metabolic Drugs.
Specimen part, Cell line
View SamplesThe role of PGC1alpha in breast cancer lung metastasis is largely unknown. We used expression data from lung metastasis of mice injected with PGC1alpha overexpression or control cells to understand global changes that occur upon overexpression of PGC1alpha that lead to lung metastasis.
PGC-1α Promotes Breast Cancer Metastasis and Confers Bioenergetic Flexibility against Metabolic Drugs.
Specimen part, Cell line
View SamplesThe role of PGC1alpha in breast cancer lung metastasis is largely unknown. We used expression data from lung metastatic explants overexpressing PGC1alpha or control, treated with phenformin to understand global gene expression changes which occur in a PGC1alpha context and under phenformin treatment.
PGC-1α Promotes Breast Cancer Metastasis and Confers Bioenergetic Flexibility against Metabolic Drugs.
Specimen part, Cell line
View Samples