GEO DataSets

(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

(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

(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

(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

(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

(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

(Submitter supplied) Bromodomain and extra terminal domain (BET) inhibition reduces occupancy of BET-family proteins at promoter and enhancer sites finally leading to genome wide changes in gene transcription. We used ChIPSeq profiling to investigate genome wide changes in promoter and enhancer occupancy induced by BET inhibitors BAY 1238097 and OTX-015, respectively.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL16791

18 Samples

Download data: BW

(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

(Submitter supplied) The present study examines the impact of altering energy provision on mitochondrial biogenesis in muscle cells. C2C12 myoblasts were chronically treated with supraphysiological levels of sodium pyruvate for 72 hr. Treated cells exhibited increased mitochondrial protein expression, basal respiratory rate and maximal oxidative capacity. The increase in mitochondrial biogenesis was independent of increases in PGC-1alpha and PGC-1alpha mRNA expression. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS2265

Platform:

GPL1261

6 Samples

Download data

Analysis of C2C12 myoblasts treated with supraphysiological levels of sodium pyruvate for 72 hours. Pyruvate increases mitochondrial biogenesis in muscle myoblasts. Results provide insight into the impact of altering energy provision on mitochondrial biogenesis in muscle cells.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 agent sets

Platform:

GPL1261

Series:

GSE5497

6 Samples

Download data

(Submitter supplied) Decreased mitochondrial mass and function in muscle of diabetic patients is associated with low PGC-1alpha, a transcriptional coactivator of the mitochondrial gene program. To investigate whether reduced PGC-1alpha and oxidative capacity in muscle directly contributes to age-related glucose intolerance, we compared the genetic signatures and metabolic profiles of aging mice lacking muscle PGC-1alpha. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS4904

Platform:

GPL1261

12 Samples

Download data: CEL

Analysis of muscle from aged animals with muscle-specific Pgc-1α depletion. PGC-1alpha is a transcriptional coactivator of the mitochondrial gene program. Results provide insight into the role of Pgc-1α in the glucose intolerance and chronic systemic inflammation associated with aging.

Organism:

Mus musculus

Type:

Expression profiling by array, transformed count, 2 age, 2 genotype/variation sets

Platform:

GPL1261

Series:

GSE52550

12 Samples

Download data: CEL

(Submitter supplied) Mitochondria play an essential role in the ability of brown fat to generate heat, and the PGC-1 coactivators control several aspects of mitochondrial biogenesis. To investigate their specific roles in brown fat cells, we generated immortal preadipocyte lines from the brown adipose tissue of mice lacking PGC-1α. We could then efficiently knockdown PGC-1β expression by shRNA expression. Loss of PGC-1α did not alter brown fat differentiation but severely reduced the induction of thermogenic genes. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS2123

Platform:

GPL1261

6 Samples

Download data

(Submitter supplied) To investigate the specific role of PGC-1 coactivators in brown fat cells, we generated immortal preadipocyte lines from the brown adipose tissue of mice lacking PGC-1alpha. We could then efficiently knockdown PGC-1beta expression by shRNA expression. Loss of PGC-1alpha did not alter brown fat differentiation but severly reduced the induction of thermogenic genes. In order to assess the specific requirement for PGC-1α in the global transcriptional response to cAMP, we used Affymetrix arrays to compare the sets of genes induced in response to a 4 hr dbcAMP treatment in differentiated wt and KO cells. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS2149

Platform:

GPL1261

8 Samples

Download data

Analysis of PGC-1alpha null brown adipocytes treated with cAMP for 4 hours. PGC-1alpha is required for the thermogenic function of brown fat cells, and cAMP plays a role in thermogenesis. Results provide insight into the role of PGC-1alpha in the global transcriptional response to cAMP.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 agent, 2 genotype/variation sets

Platform:

GPL1261

Series:

GSE5041

8 Samples

Download data

Analysis of brown fat cells lacking PGC-1alpha or both PGC-1alpha and PGC-1beta. PGC-1alpha is required for the thermogenic function of brown fat cells, and PGC-1beta is the closest homolog of PGC-1alpha. Results provide insight into the specific roles of PGC-1alpha and PGC-1beta in brown fat cells.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 3 agent, 2 genotype/variation sets

Platform:

GPL1261

Series:

GSE5042

6 Samples

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(Submitter supplied) Mitochondrial oxidative function is tightly controlled to maintain energy homeostasis in response to nutrient and hormonal signals. An important cellular component in the energy sensing response is the target of rapamycin (TOR) kinase pathway; however whether and how mTOR controls mitochondrial oxidative activity is unknown. Here, we show that mTOR kinase activity stimulates mitochondrial gene expression and oxidative function. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

12 Samples

Download data: CEL

(Submitter supplied) PRC, a member of the PGC-1 coactivator family, is responsive to serum growth factors and up regulated in proliferating cells. Here, we investigated its in vivo role by stably silencing PRC expression with two different short hairpin RNAs (shRNA#1 and shRNA#4) that were lentivirally introduced into U2OS cells. ShRNA#1 transductants exhibited nearly complete knockdown of PRC protein whereas shRNA#4 transductants expressed PRC protein at approximately 15 percent of the control level. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Datasets:

GDS3531 GDS3532

Platform:

GPL6102

12 Samples

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Analysis of U2OS cells nearly completely depleted for the PGC-1-related coactivator PRC. Loss of PRC results in a severe reduction in respiratory energy production, the proliferation of structurally defective mitochondria, and a defect in cell cycle progression.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 2 protocol sets

Platform:

GPL6102

Series:

GSE14428

6 Samples

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Analysis of U2OS cells partially depleted for the PGC-1-related coactivator PRC. Loss of PRC results in a severe reduction in respiratory energy production, the proliferation of structurally defective mitochondria, and a defect in cell cycle progression.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 2 protocol sets

Platform:

GPL6102

Series:

GSE14428

6 Samples

Download data