Identification of NCOA6-associated genomic regions in 22Rv1 human prostate cancer cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA655486 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12395841.fastq.gz | Fastqsanger.gz | |||
| SRR12395842.fastq.gz | Fastqsanger.gz | |||
| SRR12395843.fastq.gz | Fastqsanger.gz |
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Project description:In this study, we aimed to characterize the suppressive role of NCOA6 in prostate cancer development, uncover the underlying molecular mechanism, and identify potential therapeutic targets for treating NCOA6 loss-induced prostate cancer. Gene expression microarray analysis and RNA-Seq analysis were performed to identify differentially expressed genes influenced by NCOA6 in 22Rv1 human prostate cancer cells and mouse prostate tumors, respectively. Pathway enrichment analysis and gene set enrichment analysis were performed to identify NCOA6-regulated signaling pathways, particually the cancer-associated pathways. ChIP-Seq analysis was further performed to identify NCOA6-associated genomic regions in 22Rv1 cells. The potential direct target genes of NCOA6 were identified by combined analysis of the gene expression profiling data and ChIP-Seq data. Finally, we identified EGFR as one of the 264 NCOA6 direct target genes and deomonstrated that NCOA6 suppressed prostate cancer progression by preventing EGFR overexpression.
2023-08-05 | GSE155756 | GEO
Project description:In this study, we aimed to characterize the suppressive role of NCOA6 in prostate cancer development, uncover the underlying molecular mechanism, and identify potential therapeutic targets for treating NCOA6 loss-induced prostate cancer. Gene expression microarray analysis and RNA-Seq analysis were performed to identify differentially expressed genes influenced by NCOA6 in 22Rv1 human prostate cancer cells and mouse prostate tumors, respectively. Pathway enrichment analysis and gene set enrichment analysis were performed to identify NCOA6-regulated signaling pathways, particually the cancer-associated pathways. ChIP-Seq analysis was further performed to identify NCOA6-associated genomic regions in 22Rv1 cells. The potential direct target genes of NCOA6 were identified by combined analysis of the gene expression profiling data and ChIP-Seq data. Finally, we identified EGFR as one of the 264 NCOA6 direct target genes and deomonstrated that NCOA6 suppressed prostate cancer progression by preventing EGFR overexpression.
2023-08-05 | GSE155754 | GEO
Project description:Activation of the inflammatory circuits occurs frequently in cancer cells. However the molecular details linking inflammation to transformation and progression are still unknown. In this study we report for the first time, that activation of the ETS factor ESE1 is a key event connecting inflammatory signaling with prostate cancer progression. We report that ESE1 is induced upon IL-1 beta stimulation by NFKB and mediates key transcriptional changes involving cell adhesion, migration and invasion. ESE1 activation in turn induces NFKB transcriptional activation and intranuclear translocation and mediates the transforming phenotypes linked to the activation of IL-1B. Transcriptional signatures and immunohistochemistry revealed that this ESE1-NFKB regulatory circuit also operates in prostate tumors, particularly in those with significant elevation of ESE1. Thus, ESE1 promotes an inflammatory feed forward loop positively leading to prostate cancer progression. Pharmacological NFKB inhibition reverted the transformed status of ESE1 cell lines providing a rationale for context-dependent therapeutic strategies in ESE1 activated tumors. These studies find a previously unrecognized link between ETS and activation of the NFKB pathway and open new avenues for prostate cancer treatment. Gene expression analysis of a control cell line (22Rv1-pcDNA3.1) and a testing cell lines (22Rv1-ESE1), with two replicates, with dye swap, performed for each sample.
2013-06-20 | E-GEOD-39668 | biostudies-arrayexpress
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
Project description:Purpose: Even in last stage of metastatic castration-resistant prostate cancer, androgen receptor (AR) signaling remains active.To derive high metastatic prostate cancer (PCa), we labeled AR-positive but castration-resistant 22Rv1 PCa cells with luciferase gene (22Rv1-Luc2) and these cells were orthotopically implanted in mouse prostate for spontaneous progression. Methods: 2 × 10^5 of luciferase-expressing 22Rv1 cells (22Rv1-Luc2) cells were implanted in the anterior prostate of nude mice. After 12-14 weeks, the host mice were necropsied and the metastases from lumbar lymph nodes and primary tumors were dissected under laminar flow. Tumor tissues were minced using sterile scalpels and further digested with Collagenase D for 1 h. The lymph node metastatic cancer cells, named 22Rv1-M1, were orthotopically reimplanted in nude mice. At 12 weeks, the secondary metastases were isolated in the lumbar lymph nodes and designated as 22Rv1-M2 cells. Suspension of 1 × 10^6 22Rv1-M2 cells in DPBS was injected into nude mice through the tail vein, and mice developed metastases (22Rv1-M3) after 6 week. This procedure was repeated once to attain the 22Rv1-M4. Results: 22Rv1-derived metastatic cell lines exhibit increased in vitro and in vivo invasion activity as the progression from 22Rv1 to M4. Transcriptomic analysis of genome-wide gene expression in the M4 tumors reveal the unique gene expression profile compared to 22Rv1 tumors. Conclusions: Transcriptomic data provide the gene network for decoding the mechanism of PCa metastasis.
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Project description:Identification of differentially expressed genes influenced by NCOA6 in 22Rv1 human prostate cancer cells
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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
2008-06-10 | GSE11132 | GEO
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Project description:In order to determine whether ONECUT2 directly regulates the AR transcriptional program, or whether the effect of ONECUT2 is a mere consequence of AR downregulation, we performed ONECUT2 ChIP-sequencing (ChIP-seq) using the 22Rv1 human castration resistant prostate cancer cell line, which expresses high levels of ONECUT2 in comparison to other human prostate cancer cell lines
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