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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

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. 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Olga Timofeeva

PROVIDER: E-GEOD-25866 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

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Expression data from DU145 cells treated with STAT3 siRNA

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

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HIP1 mediates prostate carcinogenesis and progression through STAT3 signalling

Project description:Overexpression of HIP1 has been associated with fibroblast transformation, increasing grades of prostate cancer (CaP), and biochemical relapse. Here we demonstrate cellular transformation and phenotypic effects of HIP1 overexpression in a benign prostate epithelial cell line to be dependent on STAT3 signalling. In vivo xenografts confirmed the cellular transformation phenotype and revealed serum GDF15 to be a marker of CaP in our model. STAT3 signalling was in part, dependent on HIP1 expression, in a highly invasive, metastatic and androgen receptor (AR) negative DU145 cell line, Immunohistochemistry of a large prostate tissue microarray (TMA) revealed increased HIP1 and reciprocal GDF15 expression to adversely affect outcome warranting further studies to assess HIP1 and GDF15 as biomarkers for detection and prognostication of CaP. Gene expression of PNT1a cells stably overexpressing HIP1 protein and LNCaP cells transiently overexpressing HIP1 protein were compared with their respective empty vector control cell lines using the illumina expression array platform. There were six biological replicates for each of the four different groups.

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

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HIP1 mediates prostate carcinogenesis and progression through STAT3 signalling

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

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