Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Development of gene expression profiles for murine breast tumours overexpression the transcription factor PRH

ABSTRACT: In order to establish a profile of gene expression of tumours overexpressing PRH we performed agilient microarray analysis on four 4T1 tumour samples engineered to overexpress PRH, and four control tumours with normal PRH expression. cancer, colorectal metastasis to the liver and matched healthy tissues. The tumours had recieved no treatement prior to resection. The expression profiles were compared by one colour microarray analysis between PRH overexpression and control tumours. Genes consistently differentially expressed between the groups were taken forward for further analysis. Preparation of the tumours: 4T1 cells were infected with Adenoviral-PRH or empty Adenovirus at MOI 50 for 24 hrs. Adenoviral constructs described in Kershaw, R.M., et al., PRH/HHex inhibits the migration of breast and prostate epithelial cells through direct transcriptional regulation of Endoglin. Oncogene, 2014. 33(49): p. 5592-600. Cells were washed 4x with PBS, trypsinised, washed and resuspended in Opti-mem (Invitrogen) at 1.25x106 cells/ml and kept on ice for 20-30 min before injection. Aliquots 200 μl / 2.5x105 of the cells were injected into the no. 3 fat pad of 6-8 week old female BALB/C mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE83319 | GEO | 2016/06/15

SECONDARY ACCESSION(S): PRJNA325586

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Development of gene expression profiles for murine breast tumours overexpression the transcription factor PRH

Project description:In order to establish a profile of gene expression of tumours overexpressing PRH we performed agilient microarray analysis on four 4T1 tumour samples engineered to overexpress PRH, and four control tumours with normal PRH expression. cancer, colorectal metastasis to the liver and matched healthy tissues. The tumours had recieved no treatement prior to resection. The expression profiles were compared by one colour microarray analysis between PRH overexpression and control tumours. Genes consistently differentially expressed between the groups were taken forward for further analysis. Preparation of the tumours: 4T1 cells were infected with Adenoviral-PRH or empty Adenovirus at MOI 50 for 24 hrs. Adenoviral constructs described in Kershaw, R.M., et al., PRH/HHex inhibits the migration of breast and prostate epithelial cells through direct transcriptional regulation of Endoglin. Oncogene, 2014. 33(49): p. 5592-600. Cells were washed 4x with PBS, trypsinised, washed and resuspended in Opti-memï£¨ (Invitrogen) at 1.25x106 cells/ml and kept on ice for 20-30 min before injection. Aliquots 200 Î¼l / 2.5x105 of the cells were injected into the no. 3 fat pad of 6-8 week old female BALB/C mice. Total RNA was extracted from each tumour using the Qiagen miRNAeasy kit, processed into cRNA using the Agilient low input, one colour labelling kit, hybridised onto the 8 x 66k whole human genome expression microarrays. Data was normalised in R64 and comparison matrices between matched Tumour and Healthy endothelum were constructed. Genes upregualated in all the comparisons were taken forward for further analysis.

2016-06-15 | E-GEOD-83319 | biostudies-arrayexpress

Gene expression changes following knockdown or overexpression of HHEX/PRH

Project description:Breast tumours progress from hyperplasia to ductal carcinoma in situ (DCIS) and invasive breast carcinoma (IBC). PRH/HHEX (Proline Rich Homeodomain/Haematopoietically expressed homeobox) is a transcription factor that displays both tumour suppressor and oncogenic activity in different disease contexts however, the role of PRH in breast cancer is poorly understood. To determine the consequences of PRH loss of function in breast cancer cells we generated inducible PRH depletion in MCF-7 cells. We show that PRH depletion results in increased MCF-7 cell proliferation in part at least due to increased vascular endothelial growth factor signaling. Moreover we demonstrate that PRH depletion increases the formation of breast cancer cells with cancer stem cell-like properties. Finally, and in keeping with these findings, we show that PRH over-expression inhibits the growth of mammary tumours in mice. Collectively these data indicate that PRH plays a tumour suppressive role in the breast and they provide an explanation for the finding that low PRH mRNA levels are associated with a poor prognosis in breast cancer.

2017-08-14 | GSE94865 | GEO

Specific endothelical cells govern nanoparticle entry into solid tumours

Project description:We sequenced the transcroptome of isolated nanoparticle positive and nanoparticle negative tumour endothelial cells from mouse 4T1 mammary tumours

2021-09-07 | GSE172496 | GEO

Endoglin Protein Interactome Profiling Identifies TRIM21 and Galectin-3 as New Binding Partners

Project description:Endoglin is a 180-kDa glycoprotein receptor primarily expressed by the vascular endothelium and involved in cardiovascular disease and cancer. Heterozygous mutations in the endoglin gene (ENG) cause Hereditary Hemorrhagic Telangiectasia type 1, a vascular disease that present with nose and gastrointestinal bleeding, skin and mucosa telangiectases, and arteriovenous malformations in internal organs. A circulating form of endoglin (alias soluble endoglin, sEng), proteolytically released from the membrane-bound protein, has been observed in several inflammation-related pathological conditions and appears to contribute to endothelial dysfunction and cancer development through unknown mechanisms. Membrane-bound endoglin is an auxiliary component of the TGF-β receptor complex and the extracellular region of endoglin has been shown to interact with types I and II TGF-β receptors, as well as with BMP9 and BMP10 ligands, both members of the TGF-β family. To search for novel protein interactors, we have screened a microarray containing over 9,000 unique human proteins using recombinant sEng as bait. We find that sEng binds with high affinity, at least, to 22 new proteins. Among these, we have validated the interaction of endoglin with galectin-3, a secreted member of the lectin family with capacity to bind membrane glycoproteins, and with tripartite motif-containing protein 21 (TRIM21), an E3 ubiquitin-protein ligase. Using human endothelial cells and Chinese hamster ovary cells, we showed that endoglin co-immunoprecipitates and co-localizes with galectin-3 or TRIM21. These results open new research avenues on endoglin function and regulation.

2019-09-25 | PXD015402 | Pride

Genome-wide analysis of ex vivo gene expression of 4T1 series mouse mammary tumors

Project description:Analysis of factors upregulated in highly aggressive 410.4 and 4T1 tumour cells compared to the less aggressive 4T07 tumour cells at gene expression level. The question addressed in the present study was which secreted factors are differentially expressed by these cells and therefore could account for the observed difference in fibroblast activation in these tumours. Results provide important characterisation of the ex vivo expression profiles of highly aggressive vs. non-aggressive tumour cells. 4T07, 410.4 or 4T1 cells were inoculated into the mammary fat pad of Ub-GFP mice and total RNA from FACSorted GFP-negative; CD45-negative tumour cells was isolated.

2016-01-18 | E-GEOD-50471 | biostudies-arrayexpress

FADS1/2 control lipid metabolism and ferroptosis susceptibility in triple-negative breast cancer

Project description:Analysis of factors upregulated in highly aggressive 4T1 tumour cells compared to the less aggressive 4T07 tumour cells and the non-metastatic 67NR tumour cells at gene expression level. The question addressed in the present study was which metabolic pathways are differentially activated by these cells and therefore could account for the observed difference metastatic potential of these tumours. Results provide important characterisation of the ex vivo expression profiles of highly aggressive vs. non-aggressive tumour cells. 4T07 and 4T1 tumour cell data was previously published in GSE50471.

2024-05-13 | GSE236033 | GEO

Effect of endoglin loss on embryoid bodies

Project description:Analysis of embryonic sten cell-derived embryoid bodies following endoglin knock out. Loss of endoglin leads to profound reduction of key hematopoietic regulators including SCL, LMO2, Gata2, and TGF-? signaling molecule ALK-1. Results provide insight into molecular mechanisms underlying hemangioblast and primitive hematopoietic development. Total RNA obtained from differentiated day 3 EBs of endoglin knock out ES cells were compared to wild type E14 control ES cells.

2011-05-16 | E-GEOD-29300 | biostudies-arrayexpress

Mus musculus

Project description:Development of gene expression profiles for murine breast tumours overexpression the transcription factor PRH

| PRJNA325586 | ENA

Development of gene expression profiles for murine breast tumours treated with Sunitinib

Project description:In order to establish a profile of gene expression of tumours treated with sunitinib, 4T1 breast tumours were allowed to establish in Balb/C mice for 1 week. The mice were then treated with 40 mg/kg Sunitinib in PBS and 3.72% DMSO (treatemt group) or PBS-DMSO vehicle alone (no treatment group), daily for the period of the experiment, after which the tumours were resected homogenised and subjected to CD31 microbead separation of endothelial cells and bulk tissue, both of which were subjected to agilent microarray analysis. Treated tumours greater than 250 mm3 (by caliper measurement) after 8 days of treatment were considered resistant to treatment, those smaller than this were considered sensitive to sunitinib treatment.

2016-07-06 | GSE84048 | GEO

Proteomic analysis of extracellular vesicles (EVs) from 4T1 breast cancer cells upon paclitaxel treatment

Project description:Increasing pre-clinical data suggest that chemotherapy may elicit pro-metastatic responses in breast cancer models. Primary tumours release extracellular vesicles (EVs) that can facilitate the seeding and growth of metastatic cancer cells in distant organs, but the effects of chemotherapy on pro-metastatic EVs are poorly understood. The goal of the project was to analyse the protein content in EVs released by the mouse breast cancer cell line 4T1 after treatment with the chemotherapeutic agent paclitaxel (PTX) or its vehicle control cremophor (CREMO).

2019-01-02 | PXD010362 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data