Expression data of PTEN deficient PKO cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA975844 | ENA |
REPOSITORIES: ENA
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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
Project description:PTEN is a tumor suppressor that is often inactivated in cancer and possesses both lipid and protein phosphatase activities. We report the metabolic regulator PDHK1 (pyruvate dehydrogenase kinase1) is a synthetic-essential gene in PTEN-deficient cancer and normal cells. The predominant mechanism of PDHK1 regulation and dependency is the PTEN protein phosphatase dephosphorylates NFkB activating protein (NKAP) and limits NFkB activation to suppress expression of PDHK1, a NFkB target gene. Loss of the PTEN protein phosphatase upregulates PDHK1 to drive aerobic glycolysis and induce PDHK1 cellular dependence. PTEN-deficient human tumors harbor increased PDHK1, which is a biomarker of decreased patient survival, establishing clinical relevance. This study uncovers a PTEN-regulated signaling pathway and reveals PDHK1 as a potential target in PTEN-deficient cancers.
2019-09-09 | PXD014707 | Pride
Project description:Microarray analysis of WT (Pten2fl/fl:Shp2fl/fl:Alb-Cre-), SKO (Shp2hep-/-, or Shp2fl/fl:Alb-Cre+), PKO (Ptenhep-/-, or Pten2fl/fl:Alb-Cre+) and DKO (Ptenfl/fl:Shp2fl/fl:Alb-Cre+) liver samples to gain global molecular insights how shp2 and pten is involved in liver tumorigenesis.
2016-12-13 | GSE74732 | GEO
Project description:PTEN, a well-known tumor suppressor, negatively regulates the PI3K-AKT signaling pathway. Its loss is prevalent across various cancer types and leads to significant changes in cellular signaling networks. In this study, we investigate the effects of PTEN loss on both canonical PI3K-AKT and noncanonical tyrosine kinase pathways in MCF10A PTEN knockout (KO) cells. Through quantitative proteomics and phosphoproteomics, we identified substantial changes in protein and phosphorylation profiles, including key signaling regulators such as EphA2, Src, and MEK-ERK1/2. Our findings reveal that PTEN loss not only activates PI3K-AKT signaling but also elevates tyrosine kinase signaling, with Src kinase playing a crucial role in upregulating EphA2, an RTK implicated in tumor progression. Interestingly, inhibition of AKT alone did not consistently reduce EphA2 levels, highlighting an AKT-independent mechanism of EphA2 regulation via Src in PTEN-deficient cells. We demonstrated that combined targeting of AKT and Src pathways using Capivasertib (AKT inhibitor) and Dasatinib (Src inhibitor) significantly suppressed proliferation and induced apoptosis in PTEN-deficient breast and endometrial cancer cell lines, with notable synergy observed in patient-derived xenograft (PDX) models. These results suggest that dual inhibition of AKT and Src could provide a promising therapeutic approach for PTEN-deficient cancers, addressing resistance limitations associated with AKT inhibition alone and improving therapeutic efficacy. This study underscores the complex regulatory mechanisms involving PTEN and highlights new possibilities for targeted combination therapies in cancers with PTEN loss.
2025-12-15 | PXD057520 | Pride
Project description:sequencing data from control and PTEN-deficient mouse brain microvascular transcriptomes
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Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to reveal dynamics of liver tumourigenesis in different mouse model and identify some key regulators that control HCC initiation or progression. We also try to define a index based on transcriptome of samples to quantify tumor development stage. Methods: mRNA profiles of wild-type (WT), hepatocyte-specific shp2 deletion (Shp2−/−) mice (SKO), hepatocyte-specific pten deletion (Pten−/−) mice (PKO), and hepatocyte-specific shp2 and pten deletion mice (DKO) were generated by deep sequencing. The sequence reads that passed quality filters were mapped to Mouse genome using STAR, and mRNA profiles were obtained using cuffdiff. Results: quanlity control of mRNA profiles showed that the data captured key features of phenotypes. Significantly changed genes, pathways, biolgocial processes, ligand and receptor, epigenetic regulators et al of SKO, PKO, DKO mice at differnet age were obtaiend. Temporal gene expression patterns during liver tumorigenesis in SKO, PKO and DKO mice were obtained. Conclusions: Our study represents the first detailed analysis of temporal transcriptomes during liver tumourigenesis, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comprehensive investigations of expression profiles.
2018-12-07 | GSE123427 | GEO
Project description:We used microarrays to assess transcriptional changes in regulatory T cells upon deletion of PTEN.
2014-08-05 | GSE60057 | GEO
Project description:T cell-specific deletion of PTEN induces premalignancy in CD4+ CD8+ (DP) immature T cells in the thymus, which progresses to the development of mature CD4+ T cell lymphomas in the lymph nodes and spleen. As part of a screen to identify factors that inhibit progression to malignancy, we compared miRNA expression in premalignant PTEN-deficient DP thymocytes versus wild-type controls. DP thymocytes were collected by cell sorting from three 9-week-old, premalignant T cell-specific PTEN-deficient mice (tPTEN-/-) and three littermate controls. miRNA expression was assessed relative to a reference pool generated from an equal mixture of all samples.
2014-04-12 | E-GEOD-56759 | biostudies-arrayexpress
Project description:Expression profiling of control and PTEN deficient cerebrovascular endothelial cells by high throughput sequencing.
2019-03-30 | GSE112373 | GEO
Project description:Transcriptional profiling of mouse Th17 cells comparing WT Th17 cells with Pten-deficient Th17 cells. Naïve CD4 T cells from each mice were cultured Th17 polarizing condition for 3 days. Goal was to determine the effects of Pten on global gene expression.
2017-08-10 | GSE102414 | GEO