Transgenic expression of polyoma virus middle T antigen in the mouse prostate gives rise to carcinoma
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE26234 | GEO | 2011/06/30
SECONDARY ACCESSION(S): PRJNA135003
REPOSITORIES: GEO
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Project description:Global gene expression profiles of ventral prostates of wild types and transgenic mice created with MT antigen normal prostate vs prostate cancer induced by MT expression
2011-06-30 | E-GEOD-26234 | biostudies-arrayexpress
Project description:MED1 is a transcriptional coactivator for gene-specific activators involved in growth and development, we were interested in identifying MED1 target genes potentially involved in prostate development by cDNA microarray. Med1 was conditional knocked out in mice prostate. We performed cDNA microarray with two sets: (1) RNA isolated from three WT ventral prostates and three MT ventral prostates; (2) RNA isolated from three WT lateral prostates and three MT lateral prostates. We used microarrays to detail the global programme of gene expression underlying how Med1 was involved in mice prostate development by regulating targeted genes expression 12 mice prostate samples were divided into two groups: (1) three WT ventral prostates and three MT ventral prostates; (2) three WT lateral prostates and three MT lateral prostates.
2015-05-22 | E-GEOD-69124 | biostudies-arrayexpress
Project description:The middle T (MT) antigen of polyomavirus has provided fundamental insights into the regulation of mammalian cell growth in vitro and important animal models for the analysis of tumor induction. The mouse mammary tumor virus (MMTV)-MT model of breast cancer has been important for probing the cellular signaling pathways in mammary tumorigenesis. MT itself has no intrinsic enzymatic activity but, rather, transforms by binding to and activating key intracellular signaling molecules, phosphatidylinositol 3-kinase (PI3-kinase) being the best studied of these. Thus, MT mimics a constitutively activated receptor tyrosine kinase (RTK). Our recent work suggests that MT signaling, like that of RTKs, is often quite dependent on cellular context in vitro. Here, we examine contextual effects on signaling in animal models as well. In this study, we generated transgenic mice in which MT is expressed in the mouse prostate under the control of an (ARR)2-Probasin promoter. All male transgenic mice displayed mouse prostatic intraepithelial neoplasia (mPIN) in the ventral and dorsal/lateral prostate as early as 8 weeks of age. Notably, during the course of tumor development over time, invasive cancer, reactive stroma, and infiltration of inflammatory cells were seen. Transcriptional profiling analyses show regulation of multiple pathways, with marked upregulation of both the NF-?B and inflammatory pathways. Comparison of expression profiles of our MT prostate model with those from an MMTV-MT breast model (23) shows both tissue-specific and tissue-independent MT effects. The signature of genes regulated by MT in a tissue-independent manner may have prognostic value.
| S-EPMC3094993 | biostudies-literature
Project description:MED1 is a transcriptional coactivator for gene-specific activators involved in growth and development, we were interested in identifying MED1 target genes potentially involved in prostate development by cDNA microarray. Med1 was conditional knocked out in mice prostate. We performed cDNA microarray with two sets: (1) RNA isolated from three WT ventral prostates and three MT ventral prostates; (2) RNA isolated from three WT lateral prostates and three MT lateral prostates. We used microarrays to detail the global programme of gene expression underlying how Med1 was involved in mice prostate development by regulating targeted genes expression
2015-05-22 | GSE69124 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE30864: Gene expression of polyoma middle T antigen induced mammary tumors [AKXD x PyMT] GSE30865: Gene expression of polyoma middle T antigen induced mammary tumors [NZB x PyMT] GSE31223: Gene expression of polyoma middle T antigen induced mammary tumors [RNA_Seq : MOLF x PyMT] Refer to individual Series
2011-07-21 | E-GEOD-30866 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2011-07-22 | GSE30866 | GEO
Project description:We performed expression mouse profiling of prostates of 3 month WT, ERG, PTEN f/f and Pten f/f;ERG mice. For WT and ERG prostates, entire prostates were dissected and total RNA immediated harvested. For Pten f/f and Pten f/f;ERG prostates, the Ventral Lobe was dissected.
2013-05-10 | GSE46799 | GEO
Project description:IntroductionThe actin binding protein Mammalian enabled (Mena), has been implicated in the metastatic progression of solid tumors in humans. Mena expression level in primary tumors is correlated with metastasis in breast, cervical, colorectal and pancreatic cancers. Cells expressing high Mena levels are part of the tumor microenvironment for metastasis (TMEM), an anatomical structure that is predictive for risk of breast cancer metastasis. Previously we have shown that forced expression of Mena adenocarcinoma cells enhances invasion and metastasis in xenograft mice. Whether Mena is required for tumor progression is still unknown. Here we report the effects of Mena deficiency on tumor progression, metastasis and on normal mammary gland development.MethodsTo investigate the role of Mena in tumor progression and metastasis, Mena deficient mice were intercrossed with mice carrying a transgene expressing the polyoma middle T oncoprotein, driven by the mouse mammary tumor virus. The progeny were investigated for the effects of Mena deficiency on tumor progression via staging of primary mammary tumors and by evaluation of morbidity. Stages of metastatic progression were investigated using an in vivo invasion assay, intravital multiphoton microscopy, circulating tumor cell burden, and lung metastases. Mammary gland development was studied in whole mount mammary glands of wild type and Mena deficient mice.ResultsMena deficiency decreased morbidity and metastatic dissemination. Loss of Mena increased mammary tumor latency but had no affect on mammary tumor burden or histologic progression to carcinoma. Elimination of Mena also significantly decreased epidermal growth factor (EGF) induced in vivo invasion, in vivo motility, intravasation and metastasis. Non-tumor bearing mice deficient for Mena also showed defects in mammary gland terminal end bud formation and branching.ConclusionsDeficiency of Mena decreases metastasis by slowing tumor progression and reducing tumor cell invasion and intravasation. Mena deficiency during development causes defects in invasive processes involved in mammary gland development. These findings suggest that functional intervention targeting Mena in breast cancer patients may provide a valuable treatment option to delay tumor progression and decrease invasion and metastatic spread leading to an improved prognostic outcome.
| S-EPMC3046446 | biostudies-literature
Project description:Mouse genetic crosses were established between the PyMT model of metastatic breast cancer and NZB strain. Tumors were harvested from the animals for gene expression analysis to identify genes and network modules associated with progression to distant metastatic disease. Gene expression of 68 samples from the NZB crosses were assayed on Affymetrix chips
2011-07-21 | E-GEOD-30865 | biostudies-arrayexpress
Project description:Mouse genetic crosses were established between the PyMT model of metastatic breast cancer and AKXD strain. Tumors were harvested from the animals for gene expression analysis to identify genes and network modules associated with progression to distant metastatic disease. Gene expression of 56 samples from the AKXD crosses were assayed on Affymetrix chips
2011-07-21 | E-GEOD-30864 | biostudies-arrayexpress