Yap1 ChIP-seq in Pten/Smad4-deficient mouse prostate cancer cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA682950 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13207015.fastq.gz | Fastqsanger.gz | |||
| SRR13207016.fastq.gz | Fastqsanger.gz |
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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.
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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.
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Project description:We used microarrays to detail the global gene expression and identified differentially expressed gene list between wild-type anterior prostates and Ptenpc-/- anterior prostates, Ptenpc-/-Smad4pc-/- and Ptenpc-/- anterior prostates, Ptenpc-/-p53pc-/- and Ptenpc-/- anterior prostates at 15 weeks of age. Prostate-specific Pten deletion (Ptenpc-/-) results in prostate intraepithelial neoplasia (PIN) which, following a long latency, can progress to high-grade adenocarcinoma, albeit with minimally invasive and metastatic features. To understand this feeble progression phenotype, we conducted transcriptome comparison of five Ptenpc-/- PIN relative to three wild-type anterior prostate. Moreover, Ptenpc-/-Smad4pc-/- progress to metastasis, while Ptenpc-/-p53pc-/- not progress to metastasis. To understand this phenotype difference, we conducted transcriptome comparison of five Ptenpc-/-Smad4pc-/-to five Ptenpc-/- prostate tumor, and three Ptenpc-/-p53pc-/- to five Ptenpc-/- tumor.
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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.
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Project description:PTEN loss, one of the most frequent mutations in prostate cancer (PC), is presumed to drive disease progression through AKT activation. However, two transgenic PC models with Akt activation plus Rb loss exhibited different metastatic development: Pten/RbPE:-/- mice produced systemic metastatic adenocarcinomas with high AKT2 activation, whereas RbPE:-/- mice deficient for the Src-scaffolding protein, Akap12, induced high-grade prostatic intraepithelial neoplasias and indolent lymph node dissemination, correlating with upregulated phosphotyrosyl PI3K-p85α. Using PC cells isogenic for PTEN, we show that PTEN-deficiency correlated with dependence on both p110β and AKT2 for in vitro and in vivo parameters of metastatic growth or motility, and with downregulation of SMAD4, a known PC metastasis suppressor. In contrast, PTEN expression, which dampened these oncogenic behaviors, correlated with greater dependence on p110α plus AKT1. Our data suggest that metastatic PC aggressiveness is controlled by specific PI3K/AKT isoform combinations influenced by divergent Src activation or PTEN-loss pathways.
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Project description:PB-Cre/Pten/Smad4 mouse prostate cancer micorarray for CRPC and lung metastasis studies
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