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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE68905 | GEO | 2015/12/31

SECONDARY ACCESSION(S): PRJNA283993

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]

2015-12-31 | GSE68904 | GEO

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 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

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

| PRJNA283993 | ENA

Tgfbr2 inactivation facilitates cellular plasticity and development of Pten-null prostate cancer.

Project description:Mutations in tumors can create a state of increased cellular plasticity that promotes resistance to treatment. Thus, there is an urgent need to develop novel strategies for identifying key factors that regulate cellular plasticity in order to combat resistance to chemotherapy and radiation treatment. Here we report that prostate epithelial cell reprogramming could be exploited to identify key factors required for promoting prostate cancer tumorigenesis and cellular plasticity. Deletion of phosphatase and tensin homolog (Pten) and transforming growth factor-beta receptor type 2 (Tgfbr2) may increase prostate epithelial cell reprogramming efficiency in vitro and cause rapid tumor development and early mortality in vivo. Tgfbr2 ablation abolished TGF-? signaling but increased the bone morphogenetic protein (BMP) signaling pathway through the negative regulator Tmeff1. Furthermore, increased BMP signaling promotes expression of the tumor marker genes ID1, Oct4, Nanog, and Sox2; ID1/STAT3/NANOG expression was inversely correlated with patient survival. Thus, our findings provide information about the molecular mechanisms by which BMP signaling pathways render stemness capacity to prostate tumor cells.

| S-EPMC6161409 | biostudies-literature

Immunohistochemical detection of p53, PTEN, Rb, and p16 in canine osteosarcoma using tissue microarray.

Project description:Although inactivating mutations of tumor suppressor genes are well described in cell lines of canine osteosarcoma (OS), expression of tumor suppressor proteins in spontaneous disease is poorly characterized. We determined the immunohistochemical expression of p53, PTEN, Rb, and p16 in a large cohort of dogs with OS. Formalin-fixed, paraffin-embedded samples of canine OS were analyzed retrospectively. Primary tumor samples from 145 dogs, collected between 2003 and 2008, were evaluated by tissue microarray. Streptavidin-biotin complex immunohistochemistry was performed using monoclonal antibodies for Rb and PTEN and polyclonal antibodies for p16 and p53. The average age of dogs was 7.6 y, and 118 of 145 (81%) were purebred. Most commonly represented purebreds were Greyhound (23%), Rottweiler (11%), and Labrador Retriever (10%). Immunohistochemical detection of p53, PTEN, Rb, and p16 was 81%, 61%, 66%, and 66%, respectively. The staining pattern for p16 was primarily cytoplasmic; the predominant pattern for PTEN, Rb, and p53 was cytoplasmic and nuclear. Exclusively cytoplasmic staining was noted in 19% of samples positive for p53 and 8% of samples positive for Rb. Kaplan-Meier curves showed that protein expression was not associated with significant differences in overall survival ( p > 0.191). We documented heterogeneity in both immunostaining and subcellular localization of tumor suppressor proteins, providing further characterization of canine OS.

| S-EPMC6505918 | biostudies-literature

AKT Inhibition Modulates H3K4 Demethylase Levels in PTEN-Null Prostate Cancer.

Project description:Hyperactivated AKT kinase due to loss of its negative regulator PTEN influences many aspects of cancer biology, including chromatin. AKT primarily regulates acetyl-CoA production and phosphorylates many histone-modulating enzymes, resulting in their activation or inhibition. Therefore, understanding the therapeutic impact of AKT inhibition on chromatin-related events is essential. Here, we report that AKT inhibition in prostate-specific PTEN knockout mice significantly induces di- and trimethylation of H3K4 with concomitant reduction in H3K9 acetylation. Mechanistically, we observed that AKT inhibition reduces expression of the H3K4 methylation-specific histone demethylases KDM5 family, especially KDM5B expression at transcriptional levels. Furthermore, we observed that AKT negatively regulates miR-137 levels, which transcriptionally represses KDM5B expression. Overexpression of miR-137 significantly reduced KDM5B and increased H3K4 methylation levels but failed to change AKT phosphorylation. Overall, we observed that AKT transcriptionally regulates KDM5B mainly via repression of miR-137. Our data identify a mechanism by which AKT kinase modulates the prostate cancer epigenome through regulating H3K4 methylation. Additional studies on AKT inhibition-mediated induction of H3K4 methylation will help in designing strategies to enhance the therapeutic efficacy of PI3K/AKT inhibitors.

| S-EPMC8488980 | biostudies-literature

Mutations in the WRN gene in mice accelerate mortality in a p53-null background.

Project description:Werner's syndrome (WS) is a human disease with manifestations resembling premature aging. The gene defective in WS, WRN, encodes a DNA helicase. Here, we describe the generation of mice bearing a mutation that eliminates expression of the C terminus of the helicase domain of the WRN protein. Mutant mice are born at the expected Mendelian frequency and do not show any overt histological signs of accelerated senescence. These mice are capable of living beyond 2 years of age. Cells from these animals do not show elevated susceptibility to the genotoxins camptothecin or 4-NQO. However, mutant fibroblasts senesce approximately one passage earlier than controls. Importantly, WRN(-/-);p53(-/-) mice show an increased mortality rate relative to WRN(+/-);p53(-/-) animals. We consider possible models for the synergy between p53 and WRN mutations for the determination of life span.

| S-EPMC85622 | biostudies-literature

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