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Expression data from DU145 cells treated with STAT3 siRNA

ABSTRACT: Activation of Signal Transducer and Activator of Transcription 3 (STAT3) is common in prostate cancers. STAT3 may induce cell proliferation and resistance to apoptosis, as well as promote tumor angiogenesis, invasion, and migration by activating gene expression. Many STAT3-dependent transcriptional responses are mediated through protein-protein interactions that involve the amino-terminal domain (N-domain). In this study, we found that inhibition of the STAT3 N-domain using novel inhibitor ST3-Hel2A-2 induces apoptotic death in prostate cancer cells. The cell death was accomponied by robust activation of pro-apoptotic gene. Using chromatin immunoprecipitation and tiling human promoter arrays (ChIP-chip), we have defined genome-wide targets of STAT3 in DU145 prostate cancer cells. We found that upregulated pro-apoptotic genes were bound by STAT3 in prostate cancer cells, and that STAT3 binding was decreased following inhibition of the STAT3 N-domain. STAT3 siRNA knockdow confirmed specificity of STAT3 binding and changes in gene expression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE25867 | GEO | 2010/12/07

SECONDARY ACCESSION(S): PRJNA142469

REPOSITORIES: GEO

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Expression data from DU145 cells treated with STAT3 siRNA

Project description:Activation of Signal Transducer and Activator of Transcription 3 (STAT3) is common in prostate cancers. STAT3 may induce cell proliferation and resistance to apoptosis, as well as promote tumor angiogenesis, invasion, and migration by activating gene expression. Many STAT3-dependent transcriptional responses are mediated through protein-protein interactions that involve the amino-terminal domain (N-domain). In this study, we found that inhibition of the STAT3 N-domain using novel inhibitor ST3-Hel2A-2 induces apoptotic death in prostate cancer cells. The cell death was accomponied by robust activation of pro-apoptotic gene. Using chromatin immunoprecipitation and tiling human promoter arrays (ChIP-chip), we have defined genome-wide targets of STAT3 in DU145 prostate cancer cells. We found that upregulated pro-apoptotic genes were bound by STAT3 in prostate cancer cells, and that STAT3 binding was decreased following inhibition of the STAT3 N-domain. STAT3 siRNA knockdow confirmed specificity of STAT3 binding and changes in gene expression. DU145 cells were treated with STAT3 siRNA or scrambled siRNA for 48hr. Total RNA has been extracted and prepared for hybridization on Affymetrix HG-U133A 2.0 arrays.

2010-12-07 | E-GEOD-25867 | biostudies-arrayexpress

Expression data from DU145 cells treated with ST3-Hel2A-2 STAT3 N-domain inhibitor coupled to analysis of genome-wide STAT3 binding sites

Project description:Activation of Signal Transducer and Activator of Transcription 3 (STAT3) is common in prostate cancers. STAT3 may induce cell proliferation and resistance to apoptosis, as well as promote tumor angiogenesis, invasion, and migration by activating gene expression. Many STAT3-dependent transcriptional responses are mediated through protein-protein interactions that involve the amino-terminal domain (N-domain). In this study, we found that inhibition of the STAT3 N-domain using novel inhibitor ST3-Hel2A-2 induces apoptotic death in prostate cancer cells. The cell death was accomponied by robust activation of pro-apoptotic gene. Using chromatin immunoprecipitation and tiling human promoter arrays (ChIP-chip), we have defined genome-wide targets of STAT3 in DU145 prostate cancer cells. We found that upregulated pro-apoptotic genes were bound by STAT3 in prostate cancer cells, and that STAT3 binding was decreased following inhibition of the STAT3 N-domain. DU145 cells were treated with ST3-Hel2A-2 or DMSO as a control for 3 hr. Total RNA has been extracted and prepared for hybridization on Affymetrix HG-U133A 2.0 arrays.

2010-12-07 | E-GEOD-25866 | biostudies-arrayexpress

Genome-Wide STAT3 binding sites in DU145 prostate cancer cells coupled to expression analysis

2010-12-09 | GSE25943 | GEO

Expression data from DU145 cells treated with ST3-Hel2A-2 STAT3 N-domain inhibitor coupled to analysis of genome-wide STAT3 binding sites

2010-12-07 | GSE25866 | GEO

Micro RNA Expression data from DU145 shDCUN1D1

Project description:Defective in Cullin Neddylation 1 Domain Containing 1 (DCUN1D1) is an E3 ligase for neddylation, a post translational process similar to, and that runs in parallel with the ubiquitin proteasome pathway. Although being established as an oncogene in various squamous cell carcinomas, the role of DCUN1D1 in prostate cancer has not been explored. Here we used microarray analysis to determine the set of genes regulated by DCUN1D1 in prostate cancer cells. Using the prostate cancer DU145 cell line as model, and a lentivirus encoding shRNA-DCUN1D1, we generated DCUN1D1 knockdown cell lines. Microarray analysis identified deregulation of key gene expression, cellular growth and proliferation, developmental, cell death and cancer pathways as possible mechanisms mediated by DCUN1D1 in prostate cancer.

2023-08-01 | GSE147820 | GEO

Macrophages induce inflammation by efferocytosis of apoptotic prostate cancer cells via HIF-1α stabilization

Project description:Clearance of apoptotic cancer cells by macrophages, known as efferocytosis, fuels the bone-metastatic growth of prostate cancer cells via pro-inflammatory and immunosuppressive mechanisms that are still unclear. In this study, single-cell transcriptomics of bone marrow macrophages undergoing efferocytosis of apoptotic prostate cancer cells revealed a significant enrichment of a cellular response to hypoxia. Here we show that efferocytic macrophages promote HIF-1α stabilization under normoxic conditions through interaction with phosphorylated STAT3. Inflammatory cytokine gene expression analysis of efferocytic HIF-1α-mutant macrophages revealed a reduced expression of the pro-tumorigenic Mif. Furthermore, stabilization of HIF-1α using the HIF-prolyl-hydroxylase inhibitor, Roxadustat, enhanced MIF expression in macrophages. Finally, macrophages treated with recombinant MIF protein activated NF-κB (p65) signaling increased the expression of pro-inflammatory cytokines. Altogether, these findings suggest that the clearance of apoptotic cancer cell by tumor-associated macrophages triggers p-STAT3/HIF-1α/MIF signaling to enhance tumor-promoting inflammation in bone, suggesting this axis as a target for metastatic prostate cancer.

2022-12-14 | GSE180638 | GEO

Transcription profiling of mouse pulmonary Alveolar Type II Cells deleted for Stat2

Project description:Deletion of Stat3 induced genes influencing protein metabolism, transport, chemotaxis and apoptosis and decreased the expression of genes mediating lipid synthesis and metabolism. Srebf1 and 2, key regulators of fatty acid and steroid biosynthesis, were decreased in Stat3D/D mice. Stat3 influenced both pro- and anti-apoptotic pathways, regulating and maintaining the balance between a subset of pro- and anti-apoptotic genes that determine cell death or survival. Akt, a known target of Stat3, participates in many Stat3 mediated pathways including Jak-Stat signaling, apoptosis, the MAPK signaling, cholesterol and fatty acid biosynthesis. Deletion of Stat3 from type II epithelial cells altered the expression of genes regulating diverse cellular processes, including cell growth and apoptosis, lipid biosynthesis and metabolism. Stat3 regulates cell formation through a complex regulatory network that likely enhances alveolar epithelial cell survival and surfactant/lipid synthesis, necessary for the protection of the lung during injury. Experiment Overall Design: To better understand the roles and molecular mechanisms by which Stat3 influences gene expression in lung, the effect of cell-selective deletion of Stat3 (Stat3D/D) on genome wide mRNA expression profiles was determined in murine type II alveolar epithelial cells. Differentially expressed genes were identified from Affymetrix Murine GeneChips analysis and subjected to gene ontology classification promoter analysis, pathway mapping and literature mining.

2008-06-15 | E-GEOD-6846 | biostudies-arrayexpress

Gene Expression and Biological Processes Influenced By Deletion of Stat3 in pulmonary Alveolar Type II Cells

2007-08-24 | GSE6846 | GEO

NanoStrong miRNA from DU145 CF and HF cells

Project description:NanoString duplicate runs were created for CF- and HF-resistant cells, and for matched parental duplicate samples corresponding to each radioresistant cell type. Prostate cancer is the second most common cause of cancer death in men, and radiotherapy is a standard curative therapy for localized disease. Unfortunately, aggressive radioresistant relapses can arise, and the molecular underpinnings of radioresistance are unknown. Modern clinical radiotherapy is evolving to deliver higher doses of radiation in fewer fractions (hypofractionation). We therefore analyzed genomic, transcriptomic and proteomic data to characterize the determinants of prostate cancer radioresistance in cells treated with both conventionally fractionated and hypofractionated radiotherapy. Independent of fractionation schedule, resistance to radiotherapy involved massive genomic instability and abrogation of DNA mismatch repair. Specific prostate cancer driver genes were modulated at the RNA and protein levels, with distinct protein subcellular responses to radiotherapy. Conventional fractionation led to a far more aggressive biomolecular response than hypofractionation. Testing pre-clinical candidates identified in cell lines, we revealed POLQ as a radiosensitizer. POLQ-modulated radioresistance in model systems and was predictive of it in large patient cohorts. Pharmacologic and genetic inhibition of POLQ re-sensitized radioresistant cells, creating signatures seen in primary patient cohorts. The molecular response to radiation is highly multi-modal, and sheds light on prostate cancer lethality.

2024-08-24 | GSE241078 | GEO

Gene expression profiles regulated by Stat5a/b vs. Stat3 in human prostate cancer cells.

Project description:Identification of the molecular changes that promote viability and metastatic behaviour of prostate cancer cells is critical for the development of improved therapeutic interventions for prostate cancer. Stat5a/b and Stat3 are both constitutively active in locally-confined and advanced prostate cancer, and both transcription factors have been reported to be critical for the viability and growth of prostate cancer cells. We used microarrays to compare gene expression profiles regulated by Stat5a/b vs. Stat3 in human prostate cancer cells. DU145 and CWR22Rv1 human prostate cancer cells were transfected with Stat3 siRNA, Stat5a/b siRNA or scramble siRNA as control. After 48 h, the cells were harvested and total RNA was prepared for Affymetrix microarrays.

2010-05-27 | E-GEOD-17482 | biostudies-arrayexpress

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