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Cross-species analysis of genome-wide regulatory networks identifies a synergistic dependency between FOXM1 and CENPF that drives prostate cancer malignancy

ABSTRACT: Analysis of the transcriptome of mouse models of prostate cancer to assemble a mouse prostate cancer interactome. To assemble the mouse prostate cancer interactome, we collected 13 distinct mice or genetically-engineered mouse models (GEMMs), which together represent the full spectrum of prostate cancer phenotypes including: normal epithelium (i.e., wild-type), low-grade PIN (i.e., Nkx3.1 and APT), high-grade PIN and adenocarcinoma (i.e., APT-P; APC; Myc; NP; Erg-P; and NP53), castration-resistant prostate cancer (i.e., NP-AI), and metastatic prostate cancer (i.e., NPB; NPK; and TRAMP). To further enhance the heterogeneity afforded by this diversity of mouse models, we pharmacologically perturbed each GEMM using 13 different drugs (or appropriate vehicle). The resulting mouse prostate tissue/tumor dataset encompassed 384 expression profiles

ORGANISM(S): Mus musculus

PROVIDER: GSE53202 | GEO | 2014/05/12

SECONDARY ACCESSION(S): PRJNA231109

REPOSITORIES: GEO

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Cross-species analysis of genome-wide regulatory networks identifies a synergistic dependency between FOXM1 and CENPF that drives prostate cancer malignancy

Project description:Analysis of the transcriptome of mouse models of prostate cancer to assemble a mouse prostate cancer interactome. To assemble the mouse prostate cancer interactome, we collected 13 distinct mice or genetically-engineered mouse models (GEMMs), which together represent the full spectrum of prostate cancer phenotypes including: normal epithelium (i.e., wild-type), low-grade PIN (i.e., Nkx3.1 and APT), high-grade PIN and adenocarcinoma (i.e., APT-P; APC; Myc; NP; Erg-P; and NP53), castration-resistant prostate cancer (i.e., NP-AI), and metastatic prostate cancer (i.e., NPB; NPK; and TRAMP). To further enhance the heterogeneity afforded by this diversity of mouse models, we pharmacologically perturbed each GEMM using 13 different drugs (or appropriate vehicle). The resulting mouse prostate tissue/tumor dataset encompassed 384 expression profiles Total RNA obtained from prostate tumors/tissues of 13 mouse models of prostate cancer treated with 13 different drugs for 5 consecutive days. Prostate tumors/tissues were harvested and processed for RNA isolation and transcriptome analysis.

2014-05-12 | E-GEOD-53202 | biostudies-arrayexpress

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Project description:Transgenic mouse models have been widely used to investigate the pathology of Alzheimer’s disease (AD). To elucidate underlying mechanisms of AD pathogenesis by amyloid beta (Aβ) and tau, we have generated a novel animal model of AD; ADLP - APT mice (Alzheimer’s Disease-Like Pathology) – carrying mutations of human amyloid precursor protein (APP), human presenilin-1 (PS1) and human tau. We profiled 9,824 proteins in the hippocampus of ADLP model mice using quantitative proteomics. To identify functional signatures in pathology of ADLP - APT mice, in-depth bioinformatics analysis was performed. For a longitudinal change of differentially expressed proteins (DEPs), we identified ADLP - APT mice hippocampal proteome in an age-dependent manner. Network maps of interactome between Aβ and tau in newly generated ADLP - APT mice reveal relationship between accelerated NFT pathology of AD and proteomic changes.

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Project description:The fibroblast growth factor receptor (FGFR) and canonical Wnt signaling pathways are important regulators of carcinogenesis; however, the interaction between these two pathways in the context of prostate cancer (PCa) has not been fully elucidated. Using novel transgenic mouse models, we describe Wnt-induced synergistic acceleration of FGFR1-driven adenocarcinoma; largely due to pronounced fibroblastic reactive stroma (RS) activation surrounding prostatic intraepithelial neoplasia (PIN) lesions in endogenous and reconstitution assays. Finally, both mouse and human RS are characterized by increases in TGF-M-NM-2 signaling heterogeneity immediately adjacent to PIN lesions; however, heterogeneity is lost during later stages of progression, likely contributing to tissue invasion. These studies confirm the importance of the FGFR1-Wnt-TGF-M-NM-2 signaling axes as driving forces behind reactive stroma and aggressive adenocarcinoma. To elucidate the mechanism behind the Wnt-accelerated FGFR1 adenocarcinoma, we performed laser capture microdissection (LCM) to separate pre-cancerous (hyperplasia and PIN) epithelia and adjacent reactive-stroma cells. We utilized frozen samples from specific time points (JOCK1, 40 weeks, Pro-Cat M-CM-^W JOCK1 and Ubi-Cat M-CM-^W JOCK1, 24 weeks) and performed gene expression profiling on the respective tissues.

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