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Development of gene sets after deleting Rb and Pten in p53 null background primary prostate cells [Rb and Pten]

ABSTRACT: Our findings suggested that cytokines were upregulated in p53 null primary prostate cells after deleting Rb and/or Pten. Rb and Pten deletion are important for prostate cancer progression.

ORGANISM(S): Mus musculus

PROVIDER: GSE68904 | GEO | 2015/12/31

SECONDARY ACCESSION(S): PRJNA283995

REPOSITORIES: GEO

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Development of gene sets after deleting Rb and Pten in p53 null background primary prostate cells [Rb and Pten]

Project description:Our findings suggested that cytokines were upregulated in p53 null primary prostate cells after deleting Rb and/or Pten. Rb and Pten deletion are important for prostate cancer progression. p53-/- Rbf/f vs p53-/- Rbâf/âf primary prostate cells. Three independent experiments were performed. p53-/- Rbf/f vs p53-/- Rbâf/âf Ptenâf/âf primary prostate cells. Four independent experiments were performed.

2015-12-31 | E-GEOD-68904 | biostudies-arrayexpress

Development of gene sets after deleting Rb in p53 null background primary prostate cells [Rb only]

Project description:Our findings suggested that cytokines were upregulated in p53 null primary prostate cells after deleting Rb. Rb deletion is important for prostate cancer progression.

2015-12-31 | GSE68903 | GEO

Development of gene sets after deleting Rb in p53 null background primary prostate cells [Rb only]

Project description:Our findings suggested that cytokines were upregulated in p53 null primary prostate cells after deleting Rb. Rb deletion is important for prostate cancer progression. p53-/- Rbf/f vs p53-/- Rbâf/âf primary prostate cells.Three independent experiments were performed.

2015-12-31 | E-GEOD-68903 | biostudies-arrayexpress

Development of gene sets after deleting Rb or Rb and Pten in p53 null background primary prostate cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2015-12-31 | GSE68905 | GEO

Development of gene sets after deleting Rb or Rb and Pten in p53 null background primary prostate cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-12-31 | E-GEOD-68905 | biostudies-arrayexpress

PLEKHS1 drives PI3Ks and remodels pathway homeostasis in PTEN-null prostate

Project description:The PIP3/PI3K network is a central regulator of metabolism and is frequently activated in cancer, commonly by loss of the PIP3/PI(3,4)P2-phosphatase, PTEN. Despite huge investment, the drivers of the PI3K network in normal tissues and how they adapt to overactivation are unclear. We find that in healthy mouse prostate PI3K activity is driven by RTK/IRS signalling and constrained by pathway-feedback. In the absence of PTEN, the network is dramatically remodelled. A poorly understood, YXXM- and PIP3/PI(3,4)P2-binding PH domain-containing, adaptor, PLEKHS1, became the dominant activator and was required to sustain PIP3, AKT-phosphorylation and growth in PTEN-null prostate. This was because PLEKHS1 evaded pathway-feedback and experienced enhanced PI3K- and SRC-family kinase-dependent phosphorylation of Y258XXM, eliciting PI3K-activation. hPLEKHS1-mRNA and activating-Y419-phosphorylation of hSRC correlated with PI3K-pathway activity in human prostate cancers. We propose that in PTEN-null cells, receptor-independent, SRC-dependent tyrosine-phosphorylation of PLEKHS1 creates positive-feedback that escapes homeostasis, drives PIP3-signalling and supports tumour progression.

2023-08-23 | PXD043239 | Pride

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.

2013-04-25 | E-GEOD-46360 | biostudies-arrayexpress

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

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. 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.

2011-05-19 | E-GEOD-24691 | biostudies-arrayexpress

Hierarchical synergy of Pten, p53 and Rb pathways in high-grade astrocytoma induced in adult brain

Project description:Mutations in the PTEN, TP53 and RB1 pathways are obligate events in the pathogenesis of human glioblastomas, the highest grade of astrocytoma. To investigate synergy between these tumor suppressors in mice, we induced various combinations of compound deletions conditionally in astrocytes and neural precursors in the mature brain. The resulting highly penetrant astrocytomas showed a spectrum of histopathological variation reminiscent of human tumors, and ranged from grade III to grade IV (glioblastoma). Secondary somatic mutations varied depending on the combination of initiating deletions and were relevant to human disease. Receptor tyrosine kinase amplifications were frequent in tumors initiated by combined conditional deletion of Pten and Tp53, but not when Rb, Pten and Tp53 were simultaneously deleted. Multiple mutations within PI3K and Rb pathways were acquired, however, Mapk activation was not consistently detected in astrocytomas. Gene expression profiling revealed striking similarities to previously described human astrocytoma subclasses. A subset of astrocytomas initiated outside of proliferative niches in the adult brain. Gene expression of 8 human brain samples including 2 normal brainstem and 6 brainstem low-grade gliomas were profiled using HG-U133 plus 2 arrays. Gene expression of 38 mouse tumor samples, including 24 Pten;p53 double knockout and 14 Pten;p53;Rb1 triple knockout, were profiled using Affymetrix Mouse Genome 430 v2 arrays. Copy number changes of 51 double knockout tumor samples were analysed using Roswell Park Cancer Institute 6.5k BAC arrays. Copy number changes of 21 triple knockout tumor samples were analysed using Agilent mouse genome CGH mocirarray 244A.

2011-03-23 | E-GEOD-22927 | biostudies-arrayexpress

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