Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The transcriptional network for cell cycle regulation in prostate cancer

ABSTRACT: Several compounds were treated on the PC-3 cell line to investigate cell cycle regulation in prostate cancer through gene expression profile data. Our study demonstrated that several compounds induced cell cycle regulation in the CRPC (Castration-Resistant Prostate Cancer) cell model.

ORGANISM(S): Homo sapiens

PROVIDER: GSE45567 | GEO | 2013/11/25

SECONDARY ACCESSION(S): PRJNA195047

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The transcriptional network for cell cycle regulation in prostate cancer

Project description:Several compounds were treated on the PC-3 cell line to investigate cell cycle regulation in prostate cancer through gene expression profile data. Our study demonstrated that several compounds induced cell cycle regulation in the CRPC (Castration-Resistant Prostate Cancer) cell model. Compounds (menthol, cineol, geraniol, icilin, linalool) were dissolved in ethanol as a vehicle at 0.1% working concentration and treated in PC-3 cells in triplicate. Vehicle-treated PC-3 cells in triplicate were used as a control.

2013-11-25 | E-GEOD-45567 | biostudies-arrayexpress

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

Epigenetic Activation and alteration of chromatin structure regulated by NSD2 in metastatic castration-resistant prostate cancer (Hi-C)

Project description:To elucidate the regulation of NSD2 in metastatic castration-resistant prostate cancer(CRPC), we performed Hi-C against castration-sensitive prostate cancer cell line LNCaP and metastatic castration-resistant prostate cancer cell lines, PC3 respectively. In metastatic CRPC, we found specific regions of activation with epigenetic changes.

2024-09-04 | GSE248627 | GEO

Epigenetic Activation and alteration of chromatin structure regulated by NSD2 in metastatic castration-resistant prostate cancer (ChIP-seq)

Project description:To elucidate the regulation of NSD2 in metastatic castration-resistant prostate cancer(CRPC), we performed ChIP-seq of H3K36me2, H3K27me3, H3K4me1, H3K4me3,H3K27ac and NSD2 against castration-sensitive prostate cancer cell line LNCaP and metastatic castration-resistant prostate cancer cell lines, PC3 and DU145, respectively. In metastatic CRPC, we found specific regions of activation with epigenetic changes.

2024-09-04 | GSE248629 | GEO

Epigenetic Activation and alteration of chromatin structure regulated by NSD2 in metastatic castration-resistant prostate cancer (RNA-seq)

2024-09-04 | GSE248628 | GEO

Role of epigenetic therapy in the modulation of tumor growth and migration in human castration resistance prostate cancer cells with neuroendocrine differentiation

Project description:Neuroendocrine transdifferentiation (NED) of prostate cancer cells and aberrant activation of survival pathways involved in tumorigenesis are among the events that lead to the development of resistance to anti-androgen therapy and are associated with poor prognosis in patients with castration resistance prostate cancer (CRPC). Most of these molecular events appear to be mediated by epigenetic mechanisms, in particular DNA methylation. In this study, we evaluated the antitumor activity and epigenetic modulation of two epigenetic drugs, 5-aza-2’-deoxycytidine (AZA) and S-adenosylmethionine (SAM) in two human CRPC cell lines with NED (NED-CRPC), DU-145 and PC-3. The effects of AZA and SAM on the cell growth proliferation, cell cycle, apoptosis, migration and genome-wide DNA methylation profiling have been evaluated through MTT assay, DNA flow cytometry with propidium iodide, and Annexin V-FITC/propidium iodide staining, wound-healing assay and Infinium450k microarray, respectively. Both epigenetic drugs showed a prominent antitumor activity in NED-CRPC cell line exerted through perturbation of cell cycle progression, induction of apoptosis and migration arrest. AZA and SAM reversed NED in DU-145 and PC-3, respectively. Moreover, AZA treatment profoundly modified DNA methylation pattern, sustaining a pervasive hypomethylation of the genome, with a relevant effect on several pathways involved in regulation of cell migration, cell proliferation and apoptosis. Among these, the Wnt/beta-catenin signaling appeared to be the most directly involved. In conclusion, both AZA and SAM showed a relevant antitumor activity on NED-CRPC cell lines. This opens a new scenario in the therapy of this lethal variant of prostate cancer.

2023-01-13 | GSE164249 | GEO

Integrative sequencing reveals alterations in untreated and castration-resistant prostate cancer

Project description:We conducted an integrative sequencing of genomic, transcriptomic and DNA methylation changes in 28 untreated (PC) and 13 castration-resistant prostate cancers (CRPC). We wanted to search for previously unannotated transcripts from the RNA-sequencing data. Transcriptome assembly uncovered 128 previously unannotated prostate cancer-associated transcripts. Trans-acting correlation analysis associated the expression of several TPCATs with prostate cancer-associated transcriptional regulators, such as ERG or AR. The strongest positive correlation was observed between ERG and transcript TPCAT-10-36067 that was expressed in a subset of PCs and CRPCs as well as ETV4-positive PC-3 and ERG-positive VCaP cells. We suppressed the expression of TPCAT-10-36067 with three different siRNAs in PC-3 cells, and studied the changes in the genome-wide expression patterns of the cell line using expression arrays. Gene Ontology enrichment analysis indicated that cell cycle, mitosis and Aurora signaling were the most extensively affected processes. Experimental assay showed that the siRNA suppression of TPCAT-10-36067 had a dramatic effect on the growth, invasiveness, and rate of apoptosis of prostate cancer cells.

2016-06-05 | GSE48211 | GEO

Spermine is a natural suppressor of AR signaling in castration-resistant prostate cancer

Project description:In castration-resistant prostate cancer (CRPC), clinical response to androgen receptor (AR) antagonists is limited mainly due to AR-variants expression and restored AR signaling. The metabolite spermine is most abundant in prostate and it decreases as prostate cancer progresses, but its functions remain poorly understood. Here, we show spermine inhibits full-length androgen receptor (AR-FL) and androgen receptor splice variant 7 (AR-V7) signaling and suppresses CRPC cell proliferation by directly binding and inhibiting protein arginine methyltransferase PRMT1. Spermine reduces H4R3me2a modification at the AR locus and suppresses AR binding as well as H3K27ac modification levels at AR target genes. Spermine supplementation restrains CRPC growth in vivo. PRMT1 inhibition also suppresses AR-FL and AR-V7 signaling and reduces CRPC growth. Collectively, we demonstrate spermine as an anticancer metabolite by inhibiting PRMT1 to transcriptionally inhibit AR-FL and AR-V7 signaling in CRPC, and we indicate spermine and PRMT1 inhibition as powerful strategies overcoming limitations of current AR-based therapies in CRPC.

2023-10-11 | MTBLS8034 | MetaboLights

DDX5 promotes prostate cancer progression and activates DNA repair pathway

Project description:The small heat shock protein Hsp27 has been long demonstrated as a major driver of Castration Resistant Prostate Cancer (CRPC) progression via an androgen receptor-independent pathway. In the light of identification of its molecular mechanisms, we found that the RNA helicase protein DDX5 was an interactor of Hsp27 and DDX5 expression was regulated by Hsp27 through its cytoprotective function. We showed that DDX5 was overexpressed in a large collection of human samples in aggressive PCs, especially CRPC. Here, we described the protein-protein interaction network of DDX5 which were identified in four human prostate cell lines (PNT1A, LNCaP, DU-145 and PC-3) representing different disease stages using immunoaffinity purification and quantitative mass spectrometry. The DDX5 interactome in CRPC cells was enriched in several functions (DNA damage response, translation, transcription, RNA stability, and DNA conformation changes) involved in disease progression. Furthermore, we found a new critical function of DDX5 in DNA damage repair in CRPC and validated the interaction of DDX5 with the DNA repair complex Ku70/Ku86 which plays a pivotal role in the NHEJ process. We also showed that DDX5 overexpression conferred resistance to DNA damage poisoners (such as irradiation and cisplatin) in CRPC, a feature that could lead to genome maintenance, tumor progression and treatment resistance.

2022-08-21 | PXD023252 | Pride

Widespread alternative polyadenylation regulation reprograms the prostate cancer cell transcriptome upon androgen receptor inhibition.

Project description:Prostate cancer (PC) onset and progression relies on the androgen receptor (AR) signaling. Anti-androgenic hormonal therapy (HT) is initially efficacious, but most patients evolve to a castration resistant stage (CRPC) for which no cure is currently available. Most proposed mechanisms of acquired resistance to HT focus on the transcriptional activity in CRPC cells. In this study, however, we have uncovered a new role of AR in alternative cleavage and polyadenylation (APA) regulation.

2022-08-12 | GSE190153 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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