Identification of differentially expressed genes influenced by NCOA6 in 22Rv1 human prostate cancer cells
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PROVIDER: PRJNA655488 | ENA |
REPOSITORIES: ENA
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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 | GSE155754 | 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 | 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 | GSE155755 | GEO
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:Differentially expressed genes of C2C12 cells influenced by murine pancreatic cancer derived exosomes
| PRJNA728076 | ENA
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: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.
2017-12-01 | GSE99857 | GEO
Project description:We overexpressed miR-642a-5p or a negative control miR-NC in 22Rv1 prostate cancer cells and subjected subsequent total RNA extracted from these samples to RNA-Sequencing to generate lists of differentially regulated genes between the two treatments.
2021-09-15 | GSE160736 | GEO
Project description:Progression to androgen independent is the main cause of death in prostate cancer, and the mechanism is still unclear. By reviewing the expression profiles of 26 prostate cancer samples in a holistic view, we found a group of genes differentially expressed in androgen independent compared with androgen dependent groups (p value< 0.01, t test). Focusing on apoptosis, proliferation, hormone and angiogenesis, we found a group of genes such as thioredoxin domain containing 5 (TXNDC5), tumor necrosis factor receptor superfamily, member 10a (TNFRSF10A), ribosomal protein S19 (RPS19) and Janus kinase 2 (JAK2) up-regulated in androgen independent prostate cancer, which could play important roles in the transition from androgen dependent to androgen independent and could be biomarkers of prognosis. The main aim was comparing the androgen dependent and androgen independent prostate cancer to identify differentially expressed genes. In addition, we added several normal prostate tissue sample for comparisons. Totally 29 experiments were performed without replicates. 3 for normal prostate tissue, 8 for androgen independent cancer and 18 for androgen dependent prostate cancer. In all experiments, the reference samples are common reference, a pool with unrelated fetal tissues.
2007-09-09 | E-GEOD-5803 | biostudies-arrayexpress
Project description:Current protocols for the screening of prostate cancer cannot accurately discriminate clinically indolent tumors from more aggressive ones. One reliable indicator of outcome has been the determination of organ-confined versus nonorgan-confined disease but even this determination is often only made following prostatectomy. This underscores the need to explore alternate avenues to enhance outcome prediction of prostate cancer patients. Fluids that are proximal to the prostate, such as expressed prostatic secretions (EPS), are attractive sources of potential prostate cancer biomarkers as these fluids likely bathe the tumor. Direct-EPS samples from 16 individuals with extracapsular (n = 8) or organ-confined (n = 8) prostate cancer were used as a discovery cohort, and were analyzed in duplicate by a nine-step MudPIT on a LTQ-Orbitrap XL mass spectrometer. A total of 624 unique proteins were identified by at least two unique peptides with a 0.2% false discovery rate. A semiquantitative spectral counting algorithm identified 133 significantly differentially expressed proteins in the discovery cohort. Integrative data mining prioritized 14 candidates, including two known prostate cancer biomarkers: prostate-specific antigen and prostatic acid phosphatase, which were significantly elevated in the direct-EPS from the organ-confined cancer group. These and five other candidates (SFN, MME, PARK7, TIMP1, and TGM4) were verified by Western blotting in an independent set of direct-EPS from patients with biochemically recurrent disease (n = 5) versus patients with no evidence of recurrence upon follow-up (n = 10). Lastly, we performed proof-of-concept SRM-MS-based relative quantification of the five candidates using unpurified heavy isotope-labeled synthetic peptides spiked into pools of EPS-urines from men with extracapsular and organ-confined prostate tumors. This study represents the first efforts to define the direct-EPS proteome from two major subclasses of prostate cancer using shotgun proteomics and verification in EPS-urine by SRM-MS.
2014-01-30 | PXD000400 | Pride