ArticleMethods (San Diego, Calif.)2015
Rapid in vivo validation of candidate drivers derived from the PTEN-mutant prostate metastasis genome.
Article in Methods (San Diego, Calif.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Combined whole-organ imaging at single-cell resolution and immunohistochemical analysis of prostate cancer and its liver and brain metastases.Cell reports · 2021Article
- SHQ1 is an ER stress response gene that facilitates chemotherapeutics-induced apoptosis via sensitizing ER-stress response.Cell death & disease · 2020Article
- The PHLPP2 phosphatase is a druggable driver of prostate cancer progression.The Journal of cell biology · 2019Article
- Virus Delivery of CRISPR Guides to the Murine Prostate for Gene Alteration.Journal of visualized experiments : JoVE · 2018Article
- Mitochondrial Complex I Inhibitors Expose a Vulnerability for Selective Killing of Pten-Null Cells.Cell reports · 2018Article
- Article
- Deletion of 3p13-14 locus spanning FOXP1 to SHQ1 cooperates with PTEN loss in prostate oncogenesis.Nature communications · 2017Article
- The nuclear transport receptor Importin-11 is a tumor suppressor that maintains PTEN protein.The Journal of cell biology · 2017Article
- Lentiviral vector-mediated insertional mutagenesis screen identifies genes that influence androgen independent prostate cancer progression and predict clinical outcome.Molecular carcinogenesis · 2016Article
- A Versatile Gene Delivery System for Efficient and Tumor Specific Gene ManipulationDiscoveries (Craiova, Romania)Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Human genome analyses have revealed that increasing gene copy number alteration is a driving force of incurable cancer of the prostate (CaP). Since most of the affected genes are hidden within large amplifications or deletions, there is a need for fast and faithful validation of drivers. However, classic genetic CaP engineering in mouse makes this a daunting task because generation, breeding based combination of alterations and non-invasive monitoring of disease are too time consuming and costly. To address the unmet need, we recently developed RapidCaP mice, which endogenously recreate human PTEN-mutant metastatic CaP based on Cre/Luciferase expressing viral infection, that is guided to Pten(loxP)/Trp53(loxP) prostate. Here we use a sensitized, non-metastatic Pten/Trp53-mutant RapidCaP system for functional validation of human metastasis drivers in a much accelerated time frame of only 3-4months. We used in vivo RNAi to target three candidate tumor suppressor genes FOXP1, RYBP and SHQ1, which reside in a frequent deletion on chromosome 3p and show that Shq1 cooperates with Pten and p53 to suppress metastasis. Our results thus demonstrate that the RapidCaP system forms a much needed platform for in vivo screening and validation of genes that drive endogenous lethal CaP.
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