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Links from GEO DataSets

Items: 15

1.

Expression data from lung metastatic explants

(Submitter supplied) The 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. We used expression data to understand the pathways and genes that may lead to lung metastasis in a PGC1alpha overexpression setting.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL23038
12 Samples
Download data: CEL, TXT
Series
Accession:
GSE99556
ID:
200099556
2.

Expression data from a lung metastatic cell line or metastatic explants in mouse and human

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array
Platforms:
GPL23038 GPL23159
40 Samples
Download data: CEL
Series
Accession:
GSE99557
ID:
200099557
3.

Expression data from lung metastasis

(Submitter supplied) The 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. We used expression data to understand the pathways and genes that may lead to lung metastasis in a PGC1alpha overexpression setting.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL23038
22 Samples
Download data: CEL, TXT
Series
Accession:
GSE99555
ID:
200099555
4.

Expression data from a human lung metastatic cell line treated with siPGC1alpha or siControl

(Submitter supplied) To understand global expression changes in a knockdown of PGC1alpha (siPGC1alpha) vs control (siControl) in a lung metastatic cell line (4175) Metabolic adaptations play a key role in fuelling tumour growth. However, less is known regarding the metabolic changes that promote cancer progression to metastatic disease. Herein, we reveal that PGC-1a expression and activity are differentially regulated depending on breast cancer metastatic sites. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL23159
6 Samples
Download data: CEL, TXT
Series
Accession:
GSE99554
ID:
200099554
5.

Next generation sequencing of human cholangiocarcinoma cells and associated stem-like component

(Submitter supplied) The goal of this study is to provide a global transcriptome profiling (RNA-seq) of stem-like subset in human cholangiocarcinoma (CCA). Functional enrichment of CCA stem-like subset was performed by 3D sphere culture (SPH) in CCA cell lines. Comparison to parental CCA cells grown as 2D monolayer is provided.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL18573 GPL21697
26 Samples
Download data: RDATA, TXT
Series
Accession:
GSE162845
ID:
200162845
6.

PGC-1α mediates mitochondrial biogenesis and oxidative phosphorylation in cancer cells to promote metastasis

(Submitter supplied) The study aimed to analyse the transcriptome of mouse cancer cells while in primary tumor, in circulation and after homing to metastatic site. The model used here is the 4T1 cancer cell orthotopic model.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6885
3 Samples
Download data: TXT
Series
Accession:
GSE37344
ID:
200037344
7.

Mutant p53 controls tumor metabolism and metastasis by regulating PGC-1α

(Submitter supplied) Mutant forms of p53 protein often possess pro-tumorigenic function, conferring increased survival and migration to tumor cells via its “gain of function” activity. Whether and how a common polymorphism in TP53 at amino acid 72 (Pro72Arg, hereafter P72 and R72) impacts this gain of function has not been determined. We show that mutant p53 enhances migration and metastasis of tumors through the ability to bind and regulate PGC-1α, and that this regulation is markedly impacted by the codon 72 polymorphism. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
11 Samples
Download data: TXT
8.

The PGC-1α/ERRα Axis Represses One-Carbon Metabolism and Promotes Sensitivity to Anti-Folate Therapy in Breast Cancer

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by array
Platforms:
GPL570 GPL11154
7 Samples
Download data: BIGWIG, CEL, CHP
Series
Accession:
GSE75877
ID:
200075877
9.

The PGC-1α/ERRα Axis Represses One-Carbon Metabolism and Promotes Sensitivity to Anti-Folate Therapy in Breast Cancer [ChIP-Seq]

(Submitter supplied) Reprogramming of cellular metabolism plays a central role in fuelling malignant transformation, and AMPK as well as the PGC-1α/ERRα axis are key regulators of this process. Intersection of gene expression and binding event datasets in breast cancer cells shows that activation of AMPK significantly increases the expression of PGC-1α/ERRα and promotes the binding of ERRα to its cognate sites. Unexpectedly, the data also reveal that ERRα, in concert with PGC-1α, negatively regulates the expression of several one-carbon metabolism genes resulting in substantial perturbations in purine biosynthesis. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
3 Samples
Download data: BIGWIG, XLSX
Series
Accession:
GSE75876
ID:
200075876
10.

The PGC-1α/ERRα Axis Represses One-Carbon Metabolism and Promotes Sensitivity to Anti-Folate Therapy in Breast Cancer [Microarray expression]

(Submitter supplied) Reprogramming of cellular metabolism plays a central role in fuelling malignant transformation, and AMPK as well as the PGC-1α/ERRα axis are key regulators of this process. Intersection of gene expression and binding event datasets in breast cancer cells shows that activation of AMPK significantly increases the expression of PGC-1α/ERRα and promotes the binding of ERRα to its cognate sites. Unexpectedly, the data also reveal that ERRα, in concert with PGC-1α, negatively regulates the expression of several one-carbon metabolism genes resulting in substantial perturbations in purine biosynthesis. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
4 Samples
Download data: CEL, CHP
Series
Accession:
GSE75727
ID:
200075727
11.

Microarray analysis of skeletal muscle in PGC1α transgenic mice

(Submitter supplied) Peroxisome proliferator-activated receptor (PPAR) γ coactivator 1α (PGC1α) is a coactivator of various nuclear receptors and other transcription factors that shows increased expression in skeletal muscle during exercise. In skeletal muscle, PGC1α is considered to be involved in contractile protein function, mitochondrial function, metabolic regulation, intracellular signaling, and transcriptional responses. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL4134
4 Samples
Download data: TXT
Series
Accession:
GSE67049
ID:
200067049
12.

Regulation of HSF1-mediated transcriptional programs by PGC-1alpha

(Submitter supplied) We examined global gene expression patterns in response to PGC-1 expression in cells derived from liver or muscle. As our study revealed regulation of HSF1 by PGC-1alpha, in some experiments we knocked-down HSF1 using siRNAs in addition to inducing PGC-1alpha expression.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array
Platforms:
GPL6246 GPL6244
19 Samples
Download data: CEL
Series
Accession:
GSE51498
ID:
200051498
13.

A metabolic co-regulator bioinformatics screen reveals that PGC1α suppresses prostate cancer metastasis

(Submitter supplied) The current view of cellular transformation and cancer progression supports the notion that cancer cells must reprogram their metabolism in order to survive and progress in different microenvironments. Master co-regulators of metabolism orchestrate the modulation of multiple metabolic pathways through transcriptional programs, and hence constitute a probabilistically parsimonious mechanism for general metabolic rewiring. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
6 Samples
Download data: TXT
Series
Accession:
GSE75193
ID:
200075193
14.

Immature low-density neutrophils exhibit metabolic flexibility that facilitates breast cancer liver metastasis

(Submitter supplied) Neutrophils play a key role in the control of metastatic progression. Neutrophils are phenotypically heterogeneous and can exert either anti- or pro-metastatic functions. Here, we demonstrate that tumor cells capable of forming liver metastases induce an accumulation of neutrophils in the peripheral blood and liver parenchyma. Cancer cell-derived G-CSF, in concert with other factors, mobilizes immature low-density neutrophils that promote liver metastasis. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
12 Samples
Download data: CSV
Series
Accession:
GSE123669
ID:
200123669
15.

Transcriptional diversity and bioenergetic shift in human breast cancer metastasis revealed by single-cell RNA sequencing

(Submitter supplied) Although metastasis remains the cause of most cancer-related mortality, mechanisms governing seeding in distal tissues are poorly understood. Here we establish a robust method for identification of global transcriptomic changes in rare metastatic cells during seeding using single-cell RNA-sequencing and patient-derived xenograft (PDX) models of breast cancer. We find that both primary tumours and micrometastases display transcriptional heterogeneity, but micrometastases harbor a distinct transcriptome program conserved across PDX models that is highly predictive of poor survival in patients. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
1707 Samples
Download data: TXT
Series
Accession:
GSE123837
ID:
200123837
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