PB-Cre/Pten/Smad4 mouse prostate cancer micorarray for CRPC and lung metastasis studies
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ABSTRACT:
PROVIDER: PRJNA686079 | ENA |
REPOSITORIES: ENA
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Project description:PB-Cre/Pten/Smad4 is a transgenic mouse model of metastatic prostate adenocarcinoma (PMID: 21289624). To study the transcriptomic alterations associated with castration-resistant prostate cancer (CRPC), the PB-Cre/Pten/Smad4 males with established prostate cancer were treated with surgical castration followed by enzalutamide-admixed diet. After about 4 weeks, dorsolateral prostate (DLP) lobes of treatment-naïve prostate tumors (N=2) and CRPC tumors (N=3) were harvested and extracted for RNA purification and microarray profiling. To further study the transcriptomic changes associated with lung metastases of the PB-Cre/Pten/Smad4/mTmG CRPC model, the PB-Cre/Pten/Smad4 males with established prostate cancer were treated with surgical castration followed by enzalutamide-admixed diet. About 3 months later, from one mouse anterior prostate (AP), dorsolateral prostate (DLP), ventral prostate (VP) and GFP+ lung metastasis nodules were each harvested for RNA purification and microarray profiling.
2020-12-18 | GSE163420 | GEO
Project description:Yap1 is a critical transcription coactivator in the Hippo pathways. However, its target genes are not well defined in prostate cancer cells. To determine the downstream transcriptional targets and pathways of Yap1 in Pten/Smad4-defiicent mouse prostate cancer cells, ChIP-seq was performed in the Pten/Smad4-deficient mouse prostate cancer cells.
2022-12-31 | GSE162747 | GEO
Project description:Lung cancer is the leading cause of cancer related death in both men and women in the United States. Recently, Smad4 was discovered to be common somatic alteration in human squamous cell lung cancer. Our goal was to delineate the role of Smad4 in lung cancer. We have shown for the first time that the ablation of Pten and Smad4 in the murine airway epithelium harbors a metastatic proximal adeno-squamous lung cancer. knockout group (PTENd/d and SMAD4d/d) and control group
2015-03-12 | E-GEOD-47116 | biostudies-arrayexpress
Project description:Lung cancer is the leading cause of cancer related death in both men and women in the United States. Recently, Smad4 was discovered to be common somatic alteration in human squamous cell lung cancer. Our goal was to delineate the role of Smad4 in lung cancer. We have shown for the first time that the ablation of Pten and Smad4 in the murine airway epithelium harbors a metastatic proximal adeno-squamous lung cancer.
2015-03-12 | GSE47116 | GEO
Project description:RM1 and Pten Smad4 are two mouse models with mesenchymal and stem like features. We applied the RNA Seq to provide the transcriptomic profiling of these two cell lines.
2019-08-01 | GSE131828 | GEO
Project description:We used microarrays to analyze the global gene expression and identified differentially expressed gene list between wild-type anterior prostates and Pb-Cre4;PtenLoxP/LoxP anterior prostates, Pb-Cre4;PtenLoxP/LoxP;LrfLoxP/LoxP anterior prostates at 12 weeks of age. Prostate-specific Pten deletion (Pb-Cre4;PtenLoxP/LoxP) results in prostate intraepithelial neoplasia (PIN) which, following a long latency, can progress to high-grade adenocarcinoma, albeit with minimally invasive and metastatic features. However, inactivation of Lrf in the prostate epithelium in combination of Pten results in aggressive prostate tumors. To understand the molecular mechanisms by which loss of Lrf promotes Pten-loss-driven prostate tumorigenesis, we conducted transcriptome comparison of three wild-type anterior prostates, three Pb-Cre4;PtenLoxP/LoxP PIN, and three Pb-Cre4;PtenLoxP/LoxP;LrfLoxP/LoxP anterior prostate tumors.
2013-05-19 | E-GEOD-46473 | biostudies-arrayexpress
Project description:ERBB2 is an oncogenic driver with frequent gene mutations and amplification in human lung tumors and is an attractive target for lung cancer therapy. However, target therapies can be improved by understanding the in vivo mechanisms regulated by ERBB2 during lung tumor development. Here, we generated genetic mouse models to show that Erbb2 loss inhibited lung tumor development induced by deletion of Pten and Smad4. Transcriptome analysis showed that Erbb2 loss suppressed the significant changes of most of the induced genes by ablation of Pten and Smad4. Overlapping with ERBB2-associated human lung cancer genes further identified those ERBB2 downstream players potentially conserved in human and mouse lung tumors. Furthermore, MED24 was identified as a crucial oncogenic target of ERBB2 in lung tumor development. Taken together, ERBB2 is required for the dysregulation of cancer-related genes, such as MED24, during lung tumor development.
2019-06-19 | GSE128620 | GEO
Project description:RNA-seq was carried out on prostate tumors from mice with prostate-conditional PTEN knockout with and without prostate-conditional FOXP1-SHQ1 locus deletion (12 month old PTEN-flox/flox Pb-Cre4 mice and FOXP1-SHQ1-flox/flox PTEN-flox/flox Pb-Cre4 mice )
2017-09-08 | GSE83358 | GEO
Project description:To investigate the identity of the tissue origin for metastases, we compared gene expression profiles of the prostate tissues and seminal vesicles from PB-Pten-NICD mice and those of 7 lung metastases from different mice. Three respective cell lines established from primary seminal vesicle tumors, primary prostate tumors, and lung metastases in PB-Pten-NICD mice were also included in the microarray analysis. We hypothesized that the gene expression profiles of primary and metastatic tumors should resemble those of their tissue origins. We identified genes differentially expressed between the seminal vesicle and prostate tumors. The expression profiles of the two cell lines established from primary tumors resembled those of their respective tissue origins, which supports our hypothesis. The expression profile of the metastatic cell line resembled those of the prostate tumor tissues, indicating the prostate as its tissue of origin. The expression profiles of 2 metastatic specimens each resembled those of the seminal vesicle tumors and the prostate tumors, respectively, while the expression profiles of the remaining 3 samples displayed a mixed pattern. This study suggests that metastatic tumors in this model may have originated from either the prostate, or the seminal vesicles, or both.
2016-09-09 | GSE72549 | GEO
Project description:PTEN is one of the most altered tumor suppressor genes in human prostate cancer. Prostate specific-Pten-deficient mouse models develop prostate cancer eventually progressing to CRPC, also due to alterations of the tumor immune infiltrate.
2024-08-21 | GSE272965 | GEO