Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Androgen dependent gene expression profiling of the urogenital sinus

ABSTRACT: Cancer cells differentiate along specific lineages that largely determine their clinical and biologic behavior. Distinct cancer phenotypes from different cells and organs likely result from unique gene expression repertoires established during lineage commitment in the embryo and maintained after malignant transformation. We used comprehensive gene expression analysis to examine this concept in the prostate, an organ with a readily manipulable developmental program and a high propensity for cancer. We focused on gene expression changes in the murine prostate rudiment (Urogenital Sinus, UGS) at three time points during the first 48 hours of exposure to androgen, which initiates proliferation and invasion of prostate epithelial buds into surrounding mesenchyme. Keywords: time course, prostate gland development Differential gene expression was assessed by direct comparisons of labeled moieties, using dye-swaps as technical replicates. Hybridizations were performed on the Agilent (Santa Clara, CA) Whole Mouse Genome DNA microarray (mgug4122a). Three different time points were analyzed using RNA pooled from different embryos: • UGS of female embryos upon 6 hours of androgen treatment compared to UGS of vehicletreated mice (H6 comparison, 8 different slides); • UGS of female embryos upon 12 hours of androgen treatment compared to UGS of vehicletreated mice (H12 comparison, 6 different slides); • UGS of male embryos compared to UGS of female embryos (MvsF comparison, 10 different slides). Pools from male tissues were hybridized against pools from female litter-mates;

ORGANISM(S): Mus musculus

SUBMITTER: Luigi Marchionni

PROVIDER: E-GEOD-12077 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Androgen-induced programs for prostate epithelial growth and invasion arise in embryogenesis and are reactivated in cancer.

Schaeffer E M EM Marchionni L L Huang Z Z Simons B B Blackman A A Yu W W Parmigiani G G Berman D M DM

Oncogene 20080915 57

Cancer cells differentiate along specific lineages that largely determine their clinical and biologic behavior. Distinct cancer phenotypes from different cells and organs likely result from unique gene expression repertoires established in the embryo and maintained after malignant transformation. We used comprehensive gene expression analysis to examine this concept in the prostate, an organ with a tractable developmental program and a high propensity for cancer. We focused on gene expression in ...[more]

PMID: 18794802

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Project description:Studies centered at the intersection of embryogenesis and carcinogenesis have identified striking parallels involving signaling pathways that modulate both developmental and neoplastic processes. In the prostate, reciprocal interactions between epithelium and stroma are known to influence neoplasia and also exert morphogenic effects via the urogenital sinus mesenchyme. In this study, we sought to determine molecular relationships between aspects of normal prostate development and prostate carcinogenesis. We first characterized the gene expression program associated with key points of murine prostate organogenesis spanning the initial in utero induction of prostate budding through maturity. We identified a highly reproducible temporal program of gene expression that partitioned according to the broad developmental stages of prostate induction, branching morphogenesis, and secretory differentiation. Comparisons of gene expression profiles of murine prostate cancers arising in the context of genetically engineered alterations in the Pten tumor suppressor and Myc oncogene identified significant associations between the profile of branching morphogenesis and both cancer models. Further, the expression of genes comprising the branching morphogenesis program, such as PRDX4, SLC43A1, and DNMT3A, was significantly altered in human neoplastic prostate epithelium. These results indicate that components of normal developmental processes are active in prostate neoplasia and provide further rationale for exploiting molecular features of organogenesis to understand cancer phenotypes. Whole male UGS (E14.5, E15.5, E16.5, and E17.5) or separated prostate lobes (P7, P30, and DP90) were dissected from C57BL6/J mice and snap frozen in liquid nitrogen. For each biological replication, we pooled 3 to 10 mice representing one or two litters. RNA from pools of UGS or specific prostate lobes (vp, ap, and dlp) was prepared using the Qiagen RNeasy Mini kit. We included an on-column DNaseI treatment to remove contaminating DNA. Before RNA amplification, we combined equal quantities of RNA from vp, ap, and dlp for the postnatal prostate samples. We amplified 1 ug of total RNA from each sample through one round using the Arcturus RiboAmp kit. For the E14.5 UGS reference sample, a second round of amplification was done to provide enough RNA for all microarrays. Each developmental sample was hybridized against the E14.5 UGS reference sample with a dye swap, for a total of 42 arrays. Warning: the normalized data for this study which was made public on December 1, 2009, was swapped for some samples. All normalized data has now been corrected as of February 25, 2010. Raw data was not affected.

Dataset Information

Androgen dependent gene expression profiling of the urogenital sinus

Publications

Androgen-induced programs for prostate epithelial growth and invasion arise in embryogenesis and are reactivated in cancer.

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