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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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PTEN intact and NULL prostates in intact and castrate mice.

ABSTRACT: We performed expression profiling of prostates of 3 month wild-type and PTEN NULL mice and assessed the response to 3 days of castration. Seven three month old WT and PbCre x PTEN f/f (PTEN NULL) mice were used. They are in the C57B6 background. Three mice in each group were castrated. Three days after castration, the prostate were harvested and RNA isolated by standard protocols and analyzed by expression profiling.

ORGANISM(S): Mus musculus

SUBMITTER: Yu Chen

PROVIDER: E-GEOD-24691 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Reciprocal feedback regulation of PI3K and androgen receptor signaling in PTEN-deficient prostate cancer.

Carver Brett S BS Chapinski Caren C Wongvipat John J Hieronymus Haley H Chen Yu Y Chandarlapaty Sarat S Arora Vivek K VK Le Carl C Koutcher Jason J Scher Howard H Scardino Peter T PT Rosen Neal N Sawyers Charles L CL

Cancer cell 20110501 5

Prostate cancer is characterized by its dependence on androgen receptor (AR) and frequent activation of PI3K signaling. We find that AR transcriptional output is decreased in human and murine tumors with PTEN deletion and that PI3K pathway inhibition activates AR signaling by relieving feedback inhibition of HER kinases. Similarly, AR inhibition activates AKT signaling by reducing levels of the AKT phosphatase PHLPP. Thus, these two oncogenic pathways cross-regulate each other by reciprocal feed ...[more]

PMID: 21575859

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PTEN intact and NULL prostates in intact and castrate mice.

Project description:We performed expression profiling of prostates of 3 month wild-type and PTEN NULL mice and assessed the response to 3 days of castration.

2011-05-19 | GSE24691 | GEO

Response to catration in PTEN null and PTEN null ERG expressing mouse prostates

Project description:We performed expression mouse profiling of prostates of 3 month PTEN f/f and Pten f/f;R26(ERG) mice and assessed the response to 3 days of castration. Mice are in the C57B6 background. Two mice in each group were castrated. Three days after castration, the prostate were harvested and RNA isolated by standard protocols and analyzed by expression profiling.

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Expression profile of Pten loss and ERG overexpression in mouse prostate

Project description:We performed expression mouse profiling of prostates of 3 month WT, ERG, PTEN f/f and Pten f/f;ERG mice. For WT and ERG prostates, entire prostates were dissected and total RNA immediated harvested. For Pten f/f and Pten f/f;ERG prostates, the Ventral Lobe was dissected. Mice are in the C57B6 background. The prostate were harvested and RNA isolated by standard protocols and analyzed by expression profiling.

2013-05-10 | E-GEOD-46799 | biostudies-arrayexpress

Response to catration in PTEN null and PTEN null ERG expressing mouse prostates

Project description:We performed expression mouse profiling of prostates of 3 month PTEN f/f and Pten f/f;R26(ERG) mice and assessed the response to 3 days of castration.

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Cell autonomous role of PTEN in regulating castration-resistant prostate cancer growth

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Cell autonomous role of PTEN in regulating castration-resistant prostate cancer growth

Project description:Alteration of the PTEN/PI3K pathway is associated with late stage and castrate resistant prostate cancer (CRPC). However, how PTEN loss involves in CRPC development is not clear. Here we show that castration-resistant growth is an intrinsic property of Pten-null prostate cancer (CaP) cells, independent of cancer development stage.PTEN loss suppresses androgen-responsive gene expressions by modulating androgen receptor (AR) transcription factor activity. Conditional deletion of AR in the epithelium promotes the proliferation of Pten-null cancer cells, at least in part, by down-regulating androgen-responsive gene FKBP5 and preventing PHLPP-mediated AKT inhibition. Our findings identify PI3K and AR pathway crosstalk as a mechanism of CRPC development, with potentially important implications for CaP etiology and therapy Mouse embryonic fibroblasts (MEFs) carrying a tet-inducible Pten transgene were generated by retro viral infection and antibiotic selection. Cells were treated with 2 ug/ml doxycycline for 24 or 48 hours in tet-free FBS (5%)/MEF media (n=2). Reference samples were either cells before treatment (n=2). After each time point cells were washed twice with PBS and RNA trizol extracted. WT samples (n =2) were also included as a control.

2011-05-03 | E-GEOD-29010 | biostudies-arrayexpress

Expression data of PTEN deficient PKO cells

Project description:Incurable metastatic castration-resistant prostate cancer (CRPC) eventually occurs after androgen deprivation treatment. It is important to understand how CRPC initiates/progress. We generated a mouse androgen-independent prostate cancer cell line (PKO) from PTEN null and Hi-Myc transgenic mice in C57BL/6 background. Here we analyzed the expression profiles of PKO cells.

2023-08-23 | GSE233306 | GEO

Expression data from conditional Klf5 knockout Pten-null mouse prostates

Project description:KLF5 is a basic transcription factor that regulates multiple biological processes, but its function in tumorigenesis appears contradictory in the current literature, with some studies showing tumor suppressor activity and others showing tumor promoting activity. In this study, we examined the function of Klf5 in prostatic tumorigenesis using mice with prostate specific deletion of Klf5 and Pten, both of which are frequently deleted in human prostate cancer. Histological and molecular analyses demonstrated that when one Pten allele was deleted, which causes mouse intraepithelial neoplasia (mPIN), Klf5 deletion accelerated the emergence and progression of mPIN. When both Pten alleles were deleted, which causes prostate cancer, Klf5 deletion promoted tumor growth and caused more severe morphological and molecular alterations, and homozygous deletion of Klf5 was more effective than hemizygous deletion. Unexpectedly, while Klf5 deletion clearly promoted tumorigenesis in luminal cells, it actually diminished the numbers of Ck5-positive basal cells in the Pten-null tumors. Klf5 deletion also increased the cell proliferation rate in tumors with Pten deletion, which involved extensive activation of the PI3K/AKT and MAPK mitogenic signaling pathways and inactivation of the p15 cell cycle inhibitor. Global gene expression and pathway analyses demonstrated that multiple mechanisms could be responsible for the tumor promoting effect of Klf5 deletion, We used microarrays to detail the global programme of gene expression of Klf5-wildtype and Klf5-null mouse dorsal prostates under Pten-null context to figure out the differential expression profiling underlying tumorigenesis 4 Klf5-wildtype and 4 Klf5-null mouse (6 months age) dorsal prostates under Pten-null context were used for RNA extraction and hybridization on Affymetrix mouse st 1.0 array

2014-06-21 | E-GEOD-58719 | biostudies-arrayexpress

Effect of PTEN knockout on dabrafenib-trametinib treatment in A375 melanoma cells - replicate 1

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