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

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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE25943 | GEO | 2010/12/09

SECONDARY ACCESSION(S): PRJNA142515

REPOSITORIES: GEO

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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

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 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.

2010-12-07 | GSE25867 | 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

SWATH proteomic profiling of prostate cancer cells identifies NUSAP1 as a biomarker of response to Galiellalactone

Project description:Galiellalactone (GL) is a fungal metabolite that presents antitumor and anti-inflammatory activities in vitro and in vivo. Previous studies have shown that GL targets NF-KB and STAT3 pathways and induces G2/M cell cycle arrest in androgen-insensitive prostate cancer cells. In this study, we show that GL-induced cell cycle arrest is independent of the NF-KB and STAT3 pathways in DU145 and PC-3 cells, and also that GL did not affect cell cycling in androgen-sensitive prostate cancer cell such as LNCaP and 22Rv1 cells. In addition, we showed confluence resistance to GL in DU145 cells. Using a SWATH proteomic approach we identified the down-regulation of Nucleolar and spindle associated protein 1 (NUSAP1) under DU145 confluence and in LNCaP cells. Also, the inhibition of NUSAP1 by siRNAs induced resistance to GL in DU145 cells, suggesting that NUSAP1 may be a target for GL and could be useful as biomarker for responsiveness of the antitumor activity of GL.

2019-01-14 | PXD010993 | Pride

MicroRNA expression in DU145 sublines metastatic to lymph nodes

Project description:Comparison of non-coding RNA profiling by array in sublines of DU145 human prostate cancer cell lines created by in vivo cycling Cell lines created by removal and growth of metastatic human DU145 tumor cells from mouse lymph node (metastasized from prostate xenograft) for LN cells and extracted from lung after intravenous injection (ivLU cells). Cell line numebr represented number of in vivo cycles of metastatic selection

2013-10-29 | GSE51753 | GEO

Controls and CNTN1 overexpression in DU145 cells and CNTN1 knockdown in DU145 cell-derived prostate cancer stem-like cells

Project description:Prostate cancer stem-like cells were derived from DU145 cells as suspension spheres. DU145 cells were transduced with a CNTN1 over expressing retroviral vector and a control empty vector. DU145 spheres were transduced using a retroviral-based shRNA vector against CNTN1 and a scrambled control shRNA viral vector. Both cell lines were cultured over a couple of passages before RNA was collected.

2016-02-12 | E-MTAB-4118 | biostudies-arrayexpress

Overexpression of a panel of miRNA mimics in DU145 prostate cancer cells.

Project description:The role of a number of miRNAs found to be differentially expressed in prostate cancer was functionally investigated by overexpressing them in DU145 prostate cancer cells and by analyzing gene expression profiles.

2017-06-01 | GSE68883 | GEO

Analysis of gene expression in sublines of DU145 human prostate cancer cells created through in vivo metastatic selection

Project description:DU145 human prostate cancer cells were injected into the prostate of nude mice and cells metastasizing to lymph node (LN1) grown and experiment repeated to make LN2-4. DU145 human prostate cancer cells were injected into the tail vein of nude mice and cells metastasizing to lung (ivLU1) grown and experiment repeated to make ivLU2-4.

2013-10-29 | GSE51755 | GEO

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