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Links from GEO DataSets

Items: 15

1.
Full record GDS4096

Mutant p53 depletion effect on MDA-468.shp53 breast tumor cell line

Analysis of MDA-468.shp53 cells cultured under 3D conditions in the presence of DOX. These cells express a DOX-inducible shRNA targeting endogenous mutant p53. The p53-reduced cells have an invasive, highly disorganized appearance. Results provide insight into role of mutant p53 in breast cancer.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 2 growth protocol sets
Platform:
GPL6244
Series:
GSE31812
6 Samples
Download data: CEL
2.

Mutant p53 Disrupts Mammary Acinar Morphogenesis via the Mevalonate Pathway

(Submitter supplied) p53 is a frequent target for mutation in human tumors and previous studies have revealed that these missense mutant proteins can actively contribute to tumorigenesis. To elucidate how mutant p53 might contribute to mammary carcinogenesis we employed a three-dimensional (3D) culture model. In 3D culture non-malignant breast epithelial cells form structures reminiscent of acinar structures found in vivo, whereas breast cancer cells form highly disorganized and in some cases invasive structures. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS4096
Platform:
GPL6244
6 Samples
Download data: CEL, XLS
Series
Accession:
GSE31812
ID:
200031812
3.

The mevalonate pathway is required for pyrimidine synthesis and survival of p53-deficient colon cancer cells in metabolically compromised environments

(Submitter supplied) In this study, we have investigated the effect of p53 deletion on the metabolic activity of colon cancer cells exposed to metabolic stress. In order to recreate the simultaneous reduction in oxygen and nutrient availability found in tumors, we cultured cancer cells as multicellular tumor spheroids. Under these conditions, p53 deficient cancer cells activate the expression of enzymes of the mevalonate pathway via the sterol regulatory element binding protein 2 (SREBP2). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
30 Samples
Download data: TXT
Series
Accession:
GSE124189
ID:
200124189
4.

p53 Represses the Mevalonate Pathway to Mediate Tumor Suppression

(Submitter supplied) We have discovered that loss of wild-type p53 correlates with elevated expression of mevalonate pathway genes in murine liver cancer and in human tumors. Mechanistically p53 blocks activation of SREBP-2, the master transcriptional regulator of this pathway, by transcriptionally inducing the ABCA1 cholesterol transporter gene, which inhibits SREBP-2 maturation. In mice the increase in mevalonate gene expression occurs in premalignant p53-null hepatocytes at a stage when p53 is needed to actively suppress tumorigenesis. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
7 Samples
Download data: CSV
Series
Accession:
GSE121558
ID:
200121558
5.

Mechanical cues control mutant p53 stability through a Mevalonate/RhoA axis

(Submitter supplied) To investigate the genes differentially expressed upon plating on top of matrixes with different stiffness, we compared the expression profiles of MDA-MB-231 breast cancer cells plated on a stiff substrate (plastic) with the same cells plated on a soft substrate (hydrogels 0.7 kPa). Keywords: expression profiling by array
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
8 Samples
Download data: CEL
Series
Accession:
GSE93529
ID:
200093529
6.

Transcriptional profiling of lung tumour cell lines with distinct p53 mutations in the absence or presence of WT p53

(Submitter supplied) Microarray expression data generated to determine the impact of defined p53 mutations on lung cancer cell phenotypes, and on the tumour supressive responses induced by WT p53 restoration. In murine models of lung cancer, the therapeutic benefit of WT p53 restoration has been demonstrated in p53-deficient tumours (Juntilla et al, 2010; Feldser et al, 2010). However, it remains unknown if the restoration of WT p53 function is beneficial in p53 mutant tumours. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL17543
72 Samples
Download data: TXT
Series
Accession:
GSE94758
ID:
200094758
7.

MicroRNA-874 targets phosphomevalonate kinase and inhibits cancer cell growth via the mevalonate pathway

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24676 GPL18573
22 Samples
Download data: BIGWIG, TAR
Series
Accession:
GSE214509
ID:
200214509
8.

MicroRNA-874 targets phosphomevalonate kinase and inhibits cancer cell growth via the mevalonate pathway [scRNA-seq]

(Submitter supplied) The microRNA (miR) miR-874, a potential tumour suppressor, causes cell death via target gene suppression in various cancer types. Mevalonate pathway inhibition also causes cell death in breast cancer. However, the relationship between the mevalonate pathway and miR-874-induced apoptosis or its association with the tumour suppressor p53 has not been elucidated. We identified phosphomevalonate kinase (PMVK), a key mevalonate pathway enzyme, and sterol regulatory element-binding factor 2 (SREBF2), the master cholesterol biosynthesis regulator, as direct miR‑874 targets. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
4 Samples
Download data: TAR
Series
Accession:
GSE214508
ID:
200214508
9.

MicroRNA-874 targets phosphomevalonate kinase and inhibits cancer cell growth via the mevalonate pathway [bulkRNA-seq]

(Submitter supplied) The microRNA (miR) miR-874, a potential tumour suppressor, causes cell death via target gene suppression in various cancer types. Mevalonate pathway inhibition also causes cell death in breast cancer. However, the relationship between the mevalonate pathway and miR-874-induced apoptosis or its association with the tumour suppressor p53 has not been elucidated. We identified phosphomevalonate kinase (PMVK), a key mevalonate pathway enzyme, and sterol regulatory element-binding factor 2 (SREBF2), the master cholesterol biosynthesis regulator, as direct miR‑874 targets. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
18 Samples
Download data: BIGWIG, XLSX
Series
Accession:
GSE214507
ID:
200214507
10.

Enhancer activation during tumor progression in the KrasLSLG12D/+; Trp53LSLR172H/+; Pdx1-Cre (KPC) mouse model of pancreatic ductal adenocarcinoma.

(Submitter supplied) Murine pancreatic ductal adenocarcinoma tumor organoids (T6 and T23) were generated from primary tumors from KrasLSL-G12D/+; Trp53LSL-R172H/+; Pdx1-Cre mice. At the first passage, cells in Matrigel were overlaid with mouse complete medium alone or supplemented with 10 uM Nutlin-3a to select for cells that have undergone loss-of-heterozygosity (LOH) for the wild-type (wt, "+") allele of Trp53. Organoids were cultured for 3 passages in the presence or absense of Nutlin-3a, and then culturing was continued in unsupplemented mouse complete medium. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: BW
Series
Accession:
GSE144704
ID:
200144704
11.

Expression Analysis of Mouse Tumor and Metastatic Pancreatic Ductal Adenocarcinoma Organoids

(Submitter supplied) This study used Illumina strand-specific, paired-end RNA-sequencing to examine gene expression differences between matched murine tumor- and metastasis-derived mouse pancreatic ductal adenocarcinoma (PDAC) cells grown as three-dimensional, organoid cultures. The study analyzed 16 organoid lines derived from matched primary PDAC tumors and PDAC metastases from 6 KPC (KrasLSL-G12D; Trp53LSL-R172H; Pdx1-Cre) mice.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
16 Samples
Download data: TXT
Series
Accession:
GSE142467
ID:
200142467
12.

SOAT1 knock-out downregulates the expression of mevalonate pathway genes in PDAC organoids

(Submitter supplied) One of the emerging cancer vulnerabilities is altered metabolism, and several metabolic pathways have been shown to promote pancreatic ductal adenocarcinoma (PDAC). Here we use genetic targeting to delete SOAT1 from murine PDAC metastasis organoids, and use RNA-seq to identify genes differentially regulated in normal and cholesterol-supplemented media conditions in the presence or absence of SOAT1.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: TXT, XLS
Series
Accession:
GSE141737
ID:
200141737
13.

CD40-activation of human B cells

(Submitter supplied) Antibody-independent effector functions of B cells, such as antigen presentation and cytokine production, have been shown to play an important role in a variety of immune-mediated conditions such as autoimmune diseases, transplant rejection and graft-versus-host disease. Therapeutic strategies, which interfere with B cell activation could therefore be a useful addition to the current immunosuppressive armamentarium. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5407
Platform:
GPL96
8 Samples
Download data: CEL
Series
Accession:
GSE54017
ID:
200054017
14.
Full record GDS5407

CD40 activation effect on CD19-positive B cells

Analysis of peripheral blood-purified CD19-positive B cells activated with CD40. CD40 is a potent activation stimulus for the induction of B cell-mediated antigen presentation and cytokine production. Results provide insight into molecular mechanisms underlying B cell activation via CD40.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 4 individual, 2 protocol sets
Platform:
GPL96
Series:
GSE54017
8 Samples
Download data: CEL
DataSet
Accession:
GDS5407
ID:
5407
15.

USP28 controls SREBP2 and the mevalonate pathway to drive tumour growth in squamous cancer

(Submitter supplied) SREBP2 controls the expression of enzymes involved in the mevalonate pathway (MVP), a biosynthetic process that drives the synthesis of dolichol, heme A, ubiquinone and cholesterol but also provides substrates for protein prenylation, and that is frequently deregulated in cancer. We show here that SREBP2 is a novel substrate for the deubiquitinating enzyme USP28 and that USP28 regulates SREBP2 stability independent of FBXW7. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
15 Samples
Download data: TXT
Series
Accession:
GSE204703
ID:
200204703
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