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22RV1 prostate cancer cell line transfected with SPINK1 siRNA vs control siRNA

ABSTRACT: ETS gene fusions have been characterized in a majority of prostate cancers, however key molecular alterations in ETS negative cancers are unclear. Here we used an outlier meta-analysis (meta-COPA) to identify SPINK1 outlier-expression exclusively in a subset of ETS rearrangement negative cancers (~10% of total cases). We validated the mutual exclusivity of SPINK1 expression and ETS fusion status, demonstrated that SPINK1 outlier-expression can be detected non-invasively in urine and observed that SPINK1 outlier-expression is an independent predictor of biochemical recurrence after resection. We identified the aggressive 22RV1 cell line as a SPINK1 outlier-expression model, and demonstrate that SPINK1 knockdown in 22RV1 attenuates invasion, suggesting a functional role in ETS rearrangement negative prostate cancers. Keywords: Genetic Modification

ORGANISM(S): Homo sapiens

PROVIDER: GSE11132 | GEO | 2008/06/10

SECONDARY ACCESSION(S): PRJNA106919

REPOSITORIES: GEO

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22RV1 prostate cancer cell line transfected with SPINK1 siRNA vs control siRNA

Project description:ETS gene fusions have been characterized in a majority of prostate cancers, however key molecular alterations in ETS negative cancers are unclear. Here we used an outlier meta-analysis (meta-COPA) to identify SPINK1 outlier-expression exclusively in a subset of ETS rearrangement negative cancers (~10% of total cases). We validated the mutual exclusivity of SPINK1 expression and ETS fusion status, demonstrated that SPINK1 outlier-expression can be detected non-invasively in urine and observed that SPINK1 outlier-expression is an independent predictor of biochemical recurrence after resection. We identified the aggressive 22RV1 cell line as a SPINK1 outlier-expression model, and demonstrate that SPINK1 knockdown in 22RV1 attenuates invasion, suggesting a functional role in ETS rearrangement negative prostate cancers. Keywords: Genetic Modification 22RV1 cells were infected with non-targeting siRNA or siRNA against SPINK1. For reported hybridizations, the reference channel is 22RV1 cells infected with non-targeting siRNA. Duplicate hybridizations were performed with duplicate dye flips, for a total of four arrays. Over and under-expressed signatures were generated by filtering to include only features with significant differential expression (PValueLogRatio < 0.01) in all hybridizations and Cy5/Cy3 ratios > or < 1 in all hybridizations.

2008-06-10 | E-GEOD-11132 | biostudies-arrayexpress

Gene expression profile of 22RV1 prostate cancer cells upon SPINK1 knockdown

Project description:Serine Peptidase Inhibitor, Kazal type 1 (SPINK1) overexpression represents the second-largest prostate cancer (PCa) subtype associated with increased risk of biochemical recurrence and poor prognosis. To determine the pathways regulated by SPINK1 in 22RV1 prostate cancer cells, we performed shRNA mediated knockdown of SPINK1 using lentiviral constructs. Scrambled shRNA was used as a control. pGIPZ constructs against SPINK1 (shSPINK1-1, shSPINK1-2, shSPINK1-3) and control shScrambled construct were purchased from Dharmacon.

2019-12-16 | GSE124345 | GEO

An integrative proteomics approach to identify novel therapeutic targets for SPINK1-positive prostate cancer.

Project description:Dysregulated phosphorylation of proteins perturbs the activity of several biological pathways leading to tumorigenesis and metastases. Integrated proteomics studies offer an in-depth comprehension of cancer pathobiology, and could untangle its complex circuitries. To decipher the signaling involved in SPINK1-mediated tumorigenesis, we performed label-free quantitative proteome and phosphoproteome profiling of small hairpin RNA -mediated SPINK1 silenced (shSPINK1) and control small hairpin RNA Scrambled (shSCRM) 22RV1 cells. Our integrated proteomics data revealed ~4000 proteins and enriched ~6000 phosphopeptides in each biological replicate. Of these, 367 proteins and 807 phosphopeptides were found to be significantly altered between shSCRM and shSPINK1 cells.

2024-02-26 | PXD043086 | Pride

Gene expression profile of 22RV1 prostate cancer cells upon SPINK1 knockdown

Project description:Gene expression profile of 22RV1 prostate cancer cells upon SPINK1 knockdown

| PRJNA511709 | ENA

Polycomb Group protein EZH2-mediated transcriptional repression of microRNA-338/-421 drives SPINK1-positive prostate cancer

Project description:SPINK1 overexpression defines the second largest subtype of prostate cancer (PCa), however molecular mechanisms underlying its upregulation remains poorly understood. Here, we identified the role of miR-338-5p and miR-421 in post-transcriptional regulation of SPINK1. We established that miR-338-5p/miR-421 mediates several cellular responses against SPINK1-positive cancer by targeting oncogenic long non-coding RNA (lncRNA) MALAT1, inducing cell-cycle arrest, inhibiting epithelial-to-mesenchymal transition (EMT), cancer-stemness and drug resistance. Moreover, ectopic expression of miR-338-5p/miR-421 abrogates SPINK1-mediated oncogenesis, tumor growth and distant metastases in murine model. Importantly, RNA-sequencing expression analysis revealed an inverse correlation between miRNAs and SPINK1 or MALAT1 in PCa patients’ specimens. Further, we demonstrate Polycomb group protein EZH2-mediated epigenetic silencing of miR-338-5p/miR-421 in SPINK1-positive subtype. Thus, restoring miR-338-5p/miR-421 expression using epigenetic drugs or synthetic mimics could abrogate SPINK1-mediated oncogenesis by targeting multiple oncogenic pathways and eliciting anti-cancer pleiotropic effects. Taken together, the present study unravels the molecular mechanism underlying SPINK1 overexpression and suggests miR-338-5p and miR-421 replacement therapy for the treatment of SPINK1-positive malignancies.

2018-12-30 | GSE108558 | GEO

SPINK1 promotes Colorectal Cancer progression by down regulating Metallothioneins expression

Project description:Expression profiling was performed using Agilent Whole Human Genome Oligo Microarray (Santa Clara, CA) according to the manufacturer’s protocol. A total of 3 microarray hybridizations were performed using each stable shSPINK1 cell line samples against control shSCRM cells. SPINK1 gene was knocked down using shRNA in WIDR cells in the experimental group and shScramble cells were used as control.

2015-07-11 | E-GEOD-70761 | biostudies-arrayexpress

Effect of SPINK1 and IL-6 knockdown in JHOC9 and JHOC5 ovarian clear cell carcinoma cells

Project description:Response of JHCO9 and JHOC5 cells to infection with NT (control) lentivirus or one of two knockdown lentiviruses, SPINK1 KD or IL-6 KD.

2019-11-10 | GSE140179 | GEO

Transcriptomic Reprogramming of Prostate Cancer Cells Driven by Stroma-Derived SPINK1

Project description:Recent advances in next generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways and responses. We performed this study to investigate the transcriptome profiling (RNA-seq) of prostate cancer cells upon in vitro treatment with the conditioned media from prostate stromal cells exogenously expressing human SPINK1.

2018-08-30 | GSE108545 | GEO

Heterogeneity in the inter-tumor transcriptome of high risk prostate cancer

Project description:Background: Genomic analyses of hundreds of prostate tumors have defined a diverse landscape of mutations and genome rearrangements, but the transcriptomic effect of this complexity is less well understood, particularly at the individual tumor level. We selected a cohort of 25 high-risk prostate tumors, representing the lethal phenotype, and applied deep RNA-sequencing and matched whole genome sequencing, followed by detailed molecular characterization. Results: Ten tumors were exposed to neo-adjuvant hormone therapy and expressed marked evidence of therapy response in all except one extreme case, which demonstrated early resistance via apparent neuroendocrine transdifferentiation. We observe high inter-tumor heterogeneity, including unique sets of outlier transcripts in each tumor. Interestingly, outlier expression converged on druggable cellular pathways associated with cell cycle progression, translational control or immune regulation, suggesting distinct contemporary pathway affinity and a mechanism of tumor stratification. We characterize hundreds of novel fusion transcripts, including a high frequency of ETS fusions associated with complex genome rearrangements and the disruption of tumor suppressors. Remarkably, several tumors express unique but potentially-oncogenic non-ETS fusions, which may contribute to the phenotype of individual tumors, and have significance for disease progression. Finally, one ETS-negative tumor has a striking tandem duplication genotype which appears to be highly aggressive and present at low recurrence in ETS-negative prostate cancer, suggestive of a novel molecular subtype. Conclusions: The multitude of rare genomic and transcriptomic events detected in a high-risk tumors cohort offer novel opportunities for personalized oncology and their convergence on key pathways and functions has broad implications for precision medicine.

2014-07-21 | GSE55016 | GEO

Prostate cancer cell lines: non-targeting siRNA versus SChLAP1-siRNA treated

Project description:SChLAP1 is a novel long non-coding RNA expressed in prostate cancer. Here we performed transcriptional profiling of the prostate cancer cell lines LNCaP and 22Rv1 comparing non-targeting siRNA treatment versus SChLAP1-siRNA treatment. Goal was to determine the effect of SChLAP1 knockdown on gene expression in prostate cancer. Two-condition experiment: non-targeting siRNA versus SChLAP1 siRNA treated cells. Biological replicates: 1 control replicate, 2 treatment replicates. Technical replicates: 3 replicates per SChLAP1 siRNA. Cell lines: 22Rv1 and LNCaP.

2013-07-20 | E-GEOD-40383 | biostudies-arrayexpress

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