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Gene expression data from oncogene transformed murine prostate epithelial cell lines

ABSTRACT: Primary prostate epithelial cell cultures were established from the VENTRAL prostates of FVB mice . Cells were transduced with retroviral expression vectors encoding a single distinct oncogene (c-Myc, Ha-Ras (V-12), v-Src and NeuT, an activating mutant of ErbB2). Individual colonies of oncogene-transduced cells were selected and characterized. These cell lines demonstrate contact-independent growth characteristics in soft agar and in immune competent mice. To further characterize the molecular genetic signaling pathways regulated by specific oncogenes in prostate epithelial cells

ORGANISM(S): Mus musculus

PROVIDER: GSE37428 | GEO | 2013/04/01

SECONDARY ACCESSION(S): PRJNA159909

REPOSITORIES: GEO

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Gene expression data from oncogene transformed murine prostate epithelial cell lines

Project description:Primary prostate epithelial cell cultures were established from the VENTRAL prostates of FVB mice . Cells were transduced with retroviral expression vectors encoding a single distinct oncogene (c-Myc, Ha-Ras (V-12), v-Src and NeuT, an activating mutant of ErbB2). Individual colonies of oncogene-transduced cells were selected and characterized. These cell lines demonstrate contact-independent growth characteristics in soft agar and in immune competent mice. To further characterize the molecular genetic signaling pathways regulated by specific oncogenes in prostate epithelial cells mRNA was prepared from the oncogene transformed PEC cell lines, 12 samples(each oncogene has 3 lines) and 3 normal prostate epithelial cell controls in good condition.

2013-04-01 | E-GEOD-37428 | biostudies-arrayexpress

RNA seq analysis of AR-deleted luminal prostate epithelial cells during organogenesis

Project description:Transcriptome analysis of lineage marked AR-deleted and wild type luminal prostate epithelial cells from prostates from 4 week old males, and bulk wild-type prostates from 3 week old male mice.

2020-09-05 | GSE136982 | GEO

EMT Alters Interstitial Fluid Flow-induced Signaling in ERBB2-positive Breast Cancer

Project description:A variety of mechanotransduction forces are altered in the tumor microenvironment (TME) and these biophysical forces can influence cancer progression. One such force is interstitial fluid flow (IFF) - the movement of fluid through the tissue matrix. IFF was previously shown to induce invasion of cancer cells, but the activated signaling cascades remain poorly understood. Here, it is demonstrated that IFF induces invasion of ERBB2/HER2 expressing breast cancer cells via activation of phosphoinositide-3-kinase (PI3K). In constitutively activate ERBB2 expressing cells that have undergone epithelial-to-mesenchymal transition (EMT), IFF-mediated invasion requires the chemokine receptor CXCR4, a gradient of its ligand CXCL12, and activity of the PI3K catalytic subunits p110a and ?. In wild-type ERBB2 expressing cells, IFF-mediated invasion is chemokine receptor-independent and requires only p110a activation. To test whether cells undergoing EMT alter their signaling response to IFF, TGFb1 was used to induce EMT in wild-type ERBB2-expressing cells resulting in IFF-induced invasion dependent on CXCR4 and p110?. 2 cell lines (NeuN, NeuT), 2 conditions (flow, static), 3 replicates each, 12 samples total

2015-01-06 | E-GEOD-64670 | biostudies-arrayexpress

Identification of p130Cas/ErbB2 dependent invasive signatures in transformed mammary epithelial cells.

Project description:Understanding transcriptional changes during cancer progression is of crucial importance to develop new and more efficacious diagnostic and therapeutic approaches. It is well known that ErbB2 is over-expressed in about 25% of human invasive breast cancers. We have previously demonstrated that p130Cas over-expression synergizes with ErbB2 in mammary cell transformation and promotes ErbB2-dependent invasion in three-dimensional (3D) cultures of human mammary epithelial cells. Here, by comparing coding and non-coding gene expression profiling, we define the invasive signatures associated with concomitant p130Cas over-expression and ErbB2 activation in 3D cultures of mammary epithelial cells. Specifically, we have found that genes involved in amminoacids synthesis (CBS and PHGDH), cell motility, migration (ITPKA, PRDM1), and angiogenesis (HEY1) are up-regulated while genes involved in the inflammatory response (SAA1, S100A7) are down-regulated. In parallel, we have shown that the expression of specific miRNAs is altered. Among these, mir-200b, miR-222, miR-221and miR-424 are up-regulated while miR-27a, miR-27b and miR-23b are down-regulated. Overall this study present, for the first time, gene expression changes underlying the invasive behaviour following p130Cas over-expression in an ErbB2 transformed mammary cell model. 12 samples were analyzed: 3 ErbB2, 3 Cas, 3 Cas/ErbB2, 3 Ctr MCF10A.B2

2013-08-01 | E-GEOD-43907 | biostudies-arrayexpress

Aberrant activation of canonical Notch1 signaling in the mouse prostate drives epithelialcell proliferation and induces prostatic hyperplasiaby increasing androgen receptor sensitivity

Project description:To investigate the regulatory role of Notch1 signaling pathway in mouse prostate growth and development, we constructed mice with prostate-specific overactivation of Notch1 intracellular domain N1ICD, in which Notch1 signaling was overactivated in prostate epithelial cells. We then analyzed gene expression profiles in the prostates of overexpressed and normal Notch1 mice.

2023-04-11 | GSE200565 | GEO

Proteomic and phosphoproteomic profiling of ErbB2-dependent signalling

Project description:The mechanisms of ErbB2 signalling and the effects of its overexpression are not fully understood. Herein, SILAC expression profiling and phosphopeptide enrichment of a relevant, non-transformed, immortalized human mammary luminal epithelial cell model were used to profile ErbB2-dependent differences in protein expression and phosphorylation events triggered via EGFR (EGF treatment) and ErbB3 (HRGbeta1 treatment) in the context of ErbB2 overexpression. Bioinformatics analysis was used to infer changes in cellular processes and signalling events. We demonstrate the complexity of the responses to oncogene expression and growth factor signalling and identify protein changes relevant to ErbB2-dependent altered cellular phenotype, in particular cell cycle progression and hyper-proliferation, reduced adhesion and enhanced motility. Numerous novel sites of growth factor-regulated phosphorylation were also identified that were enhanced by ErbB2 overexpression and we putatively link these to altered cell behaviour. Moreover, we have defined a novel mechanism by which ErbB signalling suppresses basal interferon signalling that would promote the survival and proliferation of mammary luminal epithelial cells.

2018-10-26 | PXD004195 | Pride

Comparison of prostate epithelial cells from intact and castrated mice

Project description:Androgen is critical for the growth of the murine prostate. Castration removes the predominant source of androgen in the mouse, leading to prostatic atrophy and death of epithelial cells. However, studies show that epithelial cells which remain in the castrated prostate are enriched for progenitor activity compared to the intact prostate. We performed gene expression profiling of basal and luminal epithelial cells isolated from paired intact and castrated adult male C57BL/6 mouse prostates to gain insights into the mechanisms promoting survival in castration-resistant epithelial cells.

2015-12-03 | GSE75628 | GEO

Identification of p130Cas/ErbB2-dependent invasive signatures in transformed mammary epithelial cells

Project description:Understanding transcriptional changes during cancer progression is of crucial importance to develop new and more efficacious diagnostic and therapeutic approaches. It is well known that ErbB2 is overexpressed in about 25% of human invasive breast cancers. We have previously demonstrated that p130Cas overexpression synergizes with ErbB2 in mammary cell transformation and promotes ErbB2-dependent invasion in three-dimensional (3D) cultures of human mammary epithelial cells. Here, by comparing coding and non-coding gene expression profiles, we define the invasive signatures associated with concomitant p130Cas overexpression and ErbB2 activation in 3D cultures of mammary epithelial cells. Specifically, we have found that genes involved in amino acids synthesis (CBS, PHGDH), cell motility, migration (ITPKA, PRDM1), and angiogenesis (HEY1) are upregulated, while genes involved in inflammatory response (SAA1, S100A7) are downregulated. In parallel, we have shown that the expression of specific miRNAs is altered. Among these, miR-200b, miR-222, miR-221, miR-R210, and miR-424 are upregulated, while miR-27a, miR-27b, and miR-23b are downregulated. Overall, this study presents, for the first time, the gene expression changes underlying the invasive behavior following p130Cas overexpression in an ErbB2 transformed mammary cell model.

2013-07-22 | GSE42949 | GEO

Identification of p130Cas/ErbB2 dependent invasive signatures in transformed mammary epithelial cells.

2013-08-01 | GSE43907 | GEO

Identification of p130Cas/ErbB2-dependent invasive signatures in transformed mammary epithelial cells

Project description:Understanding transcriptional changes during cancer progression is of crucial importance to develop new and more efficacious diagnostic and therapeutic approaches. It is well known that ErbB2 is overexpressed in about 25% of human invasive breast cancers. We have previously demonstrated that p130Cas overexpression synergizes with ErbB2 in mammary cell transformation and promotes ErbB2-dependent invasion in three-dimensional (3D) cultures of human mammary epithelial cells. Here, by comparing coding and non-coding gene expression profiles, we define the invasive signatures associated with concomitant p130Cas overexpression and ErbB2 activation in 3D cultures of mammary epithelial cells. Specifically, we have found that genes involved in amino acids synthesis (CBS, PHGDH), cell motility, migration (ITPKA, PRDM1), and angiogenesis (HEY1) are upregulated, while genes involved in inflammatory response (SAA1, S100A7) are downregulated. In parallel, we have shown that the expression of specific miRNAs is altered. Among these, miR-200b, miR-222, miR-221, miR-R210, and miR-424 are upregulated, while miR-27a, miR-27b, and miR-23b are downregulated. Overall, this study presents, for the first time, the gene expression changes underlying the invasive behavior following p130Cas overexpression in an ErbB2 transformed mammary cell model. To identify transcriptional changes occurring during invasion we have performed a comparative microarray analysis of non coding RNA (miRNA) between MCF10A.B2 acini over-expressing p130Cas with activation of ErbB2 and control cells.

2013-07-22 | E-GEOD-42949 | biostudies-arrayexpress

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