Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MeRIP sequencing for CSPC vs CRPC samples

ABSTRACT: To investigate if there is a difference of N6-methyladenosine(m6A) modification between castration-resistant prostate cancer (CRPC) and castration-sensitive prostate cancer (CSPC), we collected 30 specimens, including 15 CRPC and 15 CSPC, to perform RNA-seq and MeRIP-seq. All specimens were postoperative tissues and each 5 CRPC or CSPC specimens were mixed into 1 sample to meet the RNA dosage of RNA-seq and MeRIP-seq.

ORGANISM(S): Homo sapiens

PROVIDER: GSE221961 | GEO | 2023/01/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcriptome profiling of Olaparib-resistant (OlapR) prostate cancer cell lines

Project description:Acquisition of resistance to the PARP inhibitor, Olaparib, constitutes a major challenge for the treatment of advanced prostate cancer. The purpose of this study was to identify molecular targets responsible for the development of acquired Olaparib resistance in advanced prostate cancer. Towards this goal, next-generation sequencing (NGS)-based gene expression profiling (RNA-Sequencing; RNA-Seq) was performed on castration-sensitive prostate cancer (CSPC)/Olaparib-sensitive LNCaP cells, castration-sensitive prostate cancer (CSPC)/Olaparib-resistant LN-OlapR cells, castration-resistant prostate cancer (CSPC)/Olaparib-sensitive C4-2B cells, and castration-resistant prostate cancer (CSPC)/Olaparib-resistant 2B-OlapR cells.

2023-12-06 | GSE249514 | GEO

PB-Cre/Pten/Smad4 mouse prostate cancer micorarray for CRPC and lung metastasis studies

Project description:PB-Cre/Pten/Smad4 is a transgenic mouse model of metastatic prostate adenocarcinoma (PMID: 21289624). To study the transcriptomic alterations associated with castration-resistant prostate cancer (CRPC), the PB-Cre/Pten/Smad4 males with established prostate cancer were treated with surgical castration followed by enzalutamide-admixed diet. After about 4 weeks, dorsolateral prostate (DLP) lobes of treatment-naïve prostate tumors (N=2) and CRPC tumors (N=3) were harvested and extracted for RNA purification and microarray profiling. To further study the transcriptomic changes associated with lung metastases of the PB-Cre/Pten/Smad4/mTmG CRPC model, the PB-Cre/Pten/Smad4 males with established prostate cancer were treated with surgical castration followed by enzalutamide-admixed diet. About 3 months later, from one mouse anterior prostate (AP), dorsolateral prostate (DLP), ventral prostate (VP) and GFP+ lung metastasis nodules were each harvested for RNA purification and microarray profiling.

2020-12-18 | GSE163420 | GEO

Expresssion data from primary mouse prostate tumor cells (primary prostate tumor cells; PPC, shrunken prostate tumor cells; S-PC, castration-resistant prostate tumor cells; CRPC)

Project description:To investigate the mechanisms underlying castration-resistant prostate cancer (CRPC) development, we used a prostate cancer (PCa) allograft mouse model. In this model, an androgen-dependent (AD) mouse prostate cancer cell line, Myc-CaP, was used. Myc-CaP cells can grow as primary prostate tumors (PPC) in immune competent FVB mice in an AD manner, when host mice are castrated, Myc-CaP allografts shrink (shrunken prostate tumor, S-PC), and later re-grow and become AR-positive CRPC. To compare the gene expression of different stage of PCa, primary cells from PPC, S-PC, and CRPC were isolated and purified. We used RNA-seq to detail the global programme of gene expression underlying castration-resistant prostate cancer (CRPC) development and identified distinct classes of up-regulated or down-regulated genes during this process.

2022-12-15 | GSE208321 | GEO

Genome-wide maps of chromatin state in patient-derived model (PDX) of AR-positive or negative CRPC

Project description:We investigated the global OCT1 genomic signals using high-throughput chromatin immunoprecipitation sequencing (ChIP-seq) in a patient-derived model (PDX) of androgen receptor (AR)-negative or positive castration resistant prostate cancer (CRPC).

2022-04-20 | GSE193073 | GEO

An androgen receptor switch underlies lineage infidelity to drive neuroendocrine prostate cancer

Project description:We generate transcription factor, histone modification and ATAC cistromes in castration-resistant prostate cancer (CRPC) and treatment-induced neuroendocrine prostate cancer (tNEPC) specimens.

2021-07-15 | GSE138460 | GEO

Analysis of the effect of androgen and androgen receptor on gene expression in CRPC model cell

Project description:Androgen receptor (AR) belongs to a nuclear receptor superfamily and functions as a ligand-dependent transcription factor. AR-regulated transcriptional program is associated with various diseases, especially prostate cancer. Suppression of AR is an effective therapy for AR-dependent prostate cancer. However, in most of the cases it relapses as castration-resistant prostate cancer (CRPC), acquiring resistance to hormone therapy. We investigated the effect of androgen treatment and AR knockdown on gene expression by RNA-seq using CRPC model cells.

2020-06-27 | GSE141806 | GEO

AR signalling in castration resistant prostate cancer (CRPC)

Project description:AR signalling in castration resistant prostate cancer (CRPC)

| PRJNA765614 | ENA

Gene expression profiling study by RNA-seq for identifying gene signatures associated with castration-refractory prostate cancer (CRPC) development.

Project description:The objective of this study is to identify gene signature associated with castration-refractory prostate cancer (CRPC) development. We carried out RNA-seq based transcriptome profiling using 45 prostate samples with various disease progression steps such as benign prostate hyperplasia (BPH), primary cancer of prostate (CaP), advanced CaP and CRPC. Via various statistical analyses, we identified significant gene set associated with each progression step and observed that AR was the only gene feature associated with all progression steps, indicating that AR is the crucial mediator of and has a diverse activity across the CaP progressions. Among the samples in this data set, there are 4 pairs of advanced CaP and CRPC samples, in which each pair was obtained from the same patient. Using these paired samples, we also determined differentially expressed genes between advanced CaP and CRPC, and performed comparative analysis of significant gene lists in matched sample pairs and in unpaired remained samples. By assessing expression difference between advanced CaP and CRPC groups, 309 and 182 genes were statistically significant in paired and unpaired samples, respectively (P < 0.001). When these two gene lists were compared, a total of 15 genes were common and applied to a number of downstream experimental assays.

2018-04-22 | GSE80609 | GEO

CRPC biomarker via proteomic analysis

Project description:Identifying biological change from hormone-naive prostate cancer to CRPC is a major clinical challenge for developing therapeutic agents. Although the pathways that lead to CRPC are not fully understood, recent evidence demonstrates that androgen signaling is often maintained through varied mechanisms. Here, we investigated PCa tissues at each stage of progression from benign prostatic hyperplasia (BPH) to CRPC based on quantitative proteomic technology, including tissues after ADT therapy. MS-based quantitative proteomics approach based on 6-plex TMT (126-131) was performed in patient tissues from T2G2 to CRPC, and benign prostatic hyperplasia (BPH) patient tissues were used as a control. We analyzed the peptide samples using two types of high resolution and accuracy mass spectrometers as LTQ orbitrap velos and Q-exactive mass spectrometer. In total, 4,768 proteins were identified in this study, among which 4,069 proteins were quantified in the combined prostate cancer tissues. Among the quantified proteins, DEPs were 865 (21.2%), those with a quantitative ratio greater than 2 were considered as upregulated, whereas those with a quantitative ratio of less than 0.5 as downregulated. Based on quantitative protein results, we performed systematic bioinformatics analysis including GO, Interpro, KEGG pathway, functional enrichment-based cluster analysis on DEPs. Finally, we found that 15 proteins including FOXA1 and HMGN1-3 between T3G3, T3GX, and CRPC were increased despite ADT treatment. Among all target, we verified increased level of FOXA1 and HMGN1-3 in CRPC by immunoblotting and indirect ELISA. In summary, we provides intracellular mechanical changes on PCa tissues according to treatment before and after ADT by mean of regulating ADT treatment. In addition, this results were identified through bioinformatics analysis, and those were suggested as potential CRPC-related factors.

2021-09-10 | PXD023592 | Pride

Stationary phase stimulon and CspC regulon

Project description:The cold shock proteins belong to a family of RNA binding proteins presenting a highly conserved domain, called cold shock domain (CSD). They are involved in various cellular processes, including adaptation to low temperature, nutritional stress, cell growth and stationary phase. Here we investigate the role of CspC in C. crescentus stationary phase and the molecular mechanisms underlying gene regulation by this protein. A global transcriptional profiling experiment comparing cspC and the wild type strain both at exponential and stationary phases was carried out. The results showed that the absence of cspC affected the transcription of 20 genes at exponential phase and 65 genes at stationary phase. Genes encoding enzymes of the glyoxylate cycle were severely downregulated in the mutant at stationary phase. The stationary phase-induced RNA binding protein CspC has an important role in gene expression at this phase. It is required for the expression of the essential gene sciP, the ECF sigma factor sigU, as well as of the genes for the glyoxylate cycle enzymes and for oxidative stress response. Two and three replicates were performed to determine the stationary phase stimulon and CspC regulon, respectively. Each replicate was conducted with an independent biological sample.

2015-08-24 | E-GEOD-61726 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data