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HIP1 mediates prostate carcinogenesis and progression through STAT3 signalling

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE35211 | GEO | 2016/09/01

SECONDARY ACCESSION(S): PRJNA150877

REPOSITORIES: GEO

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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.

2016-09-01 | E-GEOD-35211 | biostudies-arrayexpress

Role of HIP1 in HIPPI mediated transcription regulation in HeLa cells

2011-09-21 | GSE26116 | GEO

Role of HIP1 in HIPPI mediated transcription regulation in HeLa cells

Project description:Nuclear entry of transcription factor HIPPI is mediated by its interacting partner Huntingtin Interacting Protein 1 (HIP1), a nuclear localization signal containing nucleo-cytoplasmic shuttling protein. In oredr to investigate the role of HIP1 in HIPPI mediated transcriptional regulation in cell, here we performed microarray experiments using stable HIP1 knocked down HeLa cells (Hip1Si) exogenously expressing Green fluorescent protein tagged HIPPI. Total RNA extracted from HIP1 knocked down HeLa cells (Hip1Si) transfected with empty GFP vector served as control and Total RNA extracted from Hip1Si cells transfected with GFP-Hippi construct served as test. Biological replicates: 4

2011-09-20 | E-GEOD-26116 | biostudies-arrayexpress

Regulation of transcription by HIPPI and its molecular partner HIP1

Project description:This SuperSeries is composed of the following subset Series: GSE26115: Regulation of transcription by HIP1 protein interactor (HIPPI) in HeLa cells GSE26116: Role of HIP1 in HIPPI mediated transcription regulation in HeLa cells Refer to individual Series

2011-09-20 | E-GEOD-26117 | biostudies-arrayexpress

Mass Spectometry of rat synovial fibroblasts immunoprecipitated with anti-HIP1

Project description:Identify HIP1 binding proteins implicated in regulation of invasive property of Rheumatoid Arthritis (RA) fibroblast-like synoviocytes (FLS) by using FLS cell line from arthritic DA (highly invasive) and R6 (minimally invasive) arthritis-protected congenic rats, which differ in amino-acid changing HIP1 SNPs.

2024-04-18 | PXD051384 | Pride

Recurrent disruption of HIP1 identified in patients with epilepsy, learning difficulties, intellectual disability, and neurobehavioral abnormalities

Project description:We report 12 individuals from ten unrelated families with epilepsy, learning difficulties, intellectual disability, and neurobehavioral abnormalities, who segregated a microdeletion distally adjacent to the Williams-Beuren syndrome region. In six families, a recurrent ~ 1.1 Mb deletion likely resulted from nonallelic homologous recombination between flanking large complex low-copy repeats. Three smaller sized microdeletions (~ 180-500 kb) enabled us to narrow the critical region to one gene, HIP1, encoding Huntington interacting protein 1.

2010-08-28 | GSE23834 | GEO

Regulation of transcription by HIPPI and its molecular partner HIP1

Project description:Regulation of transcription by HIPPI and its molecular partner HIP1

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Recurrent disruption of HIP1 identified in patients with epilepsy, learning difficulties, intellectual disability, and neurobehavioral abnormalities

2010-08-28 | E-GEOD-23834 | biostudies-arrayexpress

Homo sapiens

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Quantitative secretomics identifies ligand-receptor pairs in pancreatic cancer that mediate bidirectional crosstalk between cancer stem cells and nociceptors

Project description:Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest and most metastatic cancers in human. PDACs respond poorly to therapies, partly due to cancer stem cells (CSCs) that self-renew, survive chemotherapies, metastasise and replenish the tumour. Factors secreted by tumour cells mediate autocrine/paracrine crosstalk with surrounding cells contributing to the stem cell niche but are still insufficiently characterised. Here we used quantitative SILAC proteomics to identify secreted factors enriched in CSC secretome compared to non-CSCs. Among them were GDF15 and VGF, factors involved in cachexia and pain stimuli. GDF15 and VGF promoted CSC self-renewal and growth through autocrine effects. TGFβ/Activin signalling lowered GDF15 and VGF expression via SMAD2/3-SMAD4-SNON, switching to ATF4-CREB-mediated induction upon cell stress. Co-culture of PDAC-CSCs and hESC-derived neural cells for mimicking cellular crosstalk in PDAC revealed that paracrine signalling via GDF15/VGF promoted nociceptor formation and neurite outgrowth. In turn, Substance P from neurons supported CSC self-renewal, EMT/migration and clonal evolution that was also impacted by SMAD4 genetic status. Lastly, the serum levels of GDF15 and VGF were elevated in PDAC patients suggesting their utility as biomarkers for PDAC detection. Collectively, our data uncovered that cachexia and pain signalling factors mediate the crosstalk between CSCs and nociceptors.

2024-04-06 | PXD046026 | Pride

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