Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Analysis of cabazitaxel-resistant mechanism in human castration-resistant prostate cancer

ABSTRACT: To investigate cabazitaxel (CBZ) resistance in prostate cancer, we examined the changes in global gene expression before and after development of acquired CBZ resistance. Functional annotation clustering (FAC) analysis of DAVID showed cell division (GO: 0051301) and mitotic nuclear division (GO: 0007067) were the most enhanced clusters in DU145CR compared with DU145.

ORGANISM(S): Homo sapiens

PROVIDER: GSE110107 | GEO | 2018/08/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Analysis of cabazitaxel-resistant mechanism in human castration-resistant prostate cancer

Project description:To investigate cabazitaxel (CBZ) resistance in prostate cancer, we examined the changes in global gene expression before and after development of acquired CBZ resistance. Functional annotation clustering (FAC) analysis of DAVID showed cell division (GO: 0051301) and mitotic nuclear division (GO: 0007067) were the most enhanced clusters in PC3CR compared with PC3.

2021-08-24 | GSE182619 | GEO

Effects of OCT4/NRF1 knockdown in castration-resistant prostate cancer cells

Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. Although initially hormone-deprovation therapy is effective to inhibit cancer progression, most of cancers relapse as castration-resistant prostate cancer (CRPC). In this study, we examined the effect of OCT4 or NRF1 knockdown in CRPC cells. In order to investigate the OCT4 and NRF1 function in CRPC cells, we performed gene expression in AR-positive CRPC cell line, 22Rv1, AR-negative CRPC cell lines, PC3-CR (Cabazitaxel resistant), DU145, and DU145-CR, after siOCT4 (10 nM) or siNRF1 (10 nM) treatment. We also treated cells with vehicle, ribavirin (riba), or dihydrotestosterone (DHT) to analyzed the effects of thiese drug treatments.

2021-05-01 | GSE146656 | GEO

Expression data from docetaxel-resistant and cabazitaxel-resistant prostate cancer cell lines

Project description:Docetaxel and cabazitaxel are the chemotherapy agents used in castration-resistant prostate cancer. However, most patients eventually develop resistance to these treatments. The aim of the study was to identify key molecular genes and networks associated with taxanes resistance in 2 models of docetaxel-resistant and cabazitaxel-resistant castration-resistant prostate cancer cell lines.

2020-10-25 | GSE158494 | GEO

CDK7 inhibition suppresses Castration-Resistant Prostate Cancer through MED1 inactivation

Project description:We performed RNA-seq and ChIP-seq in three prostate cell lines (VCaP, LNCaP and DU145) to ascertain the role of the mediator complex MED1 in AR signaling. Upon androgen stimulation, MED1 undergoes phosphorylation by CDK7 and physically engages with AR at super-enhancer sites, which is essential for AR-mediated transcription. The CDK7 specific inhibitor THZ1 blunts AR-dependent neoplastic growth by preventing the co-recruitment of AR/MED1 in a genome-wide fashion, and reverts the enzalutamide resistance characterized by hyper-phosphorylated MED1. The effect of THZ1 phenocopies that for MED1 and CDK7 knockdown.

2019-08-20 | GSE125245 | GEO

Analysis of cabazitaxel-resistant mechanism in human castration-resistant prostate cancer

Project description:Analysis of cabazitaxel-resistant mechanism in human castration-resistant prostate cancer

| PRJNA757016 | ENA

Analysis of cabazitaxel-resistant mechanism in human castration-resistant prostate cancer

Project description:Analysis of cabazitaxel-resistant mechanism in human castration-resistant prostate cancer

| PRJNA433108 | ENA

ATF6 is required for the survival of castration-resistant prostate cancer cells

Project description:To gain insight into the global ATF6 target gene profile in prostate cancer cells, we performed RNA-seq analysis in DU145 cells upon either ATF6 siRNA-mediated knockdown (siATF6) or Ceapin-A7-mediated ATF6α inhibition.

2022-03-23 | GSE199026 | GEO

Functional and Mechanistic Interrogation of BET Bromodomain Degraders for the Treatment of Metastatic Castration-resistant Prostate Cancer

Project description:RNA-seq on VCaP, 22Rv1, and DU145 cells treated with BET-inhibitors and BET-Degradaing molecules

2021-07-08 | GSE179282 | GEO

RNA-seq Analysis of Castration-Resistant Prostate Cancer With Knock-down of E2F1

Project description:From castration resistant prostate cancer (CRPC) regulatory network, we found over 90% negative feedback loop went through E2F1. And we detected PC3 and DU145 cells with depletion of E2F1 through the invasion, migration, proliferation and apoptosis experiments. In order to identify which genes trigger these phenomenon and regulatory mechanism of E2F1 in CRPC, we performed the gene expression between the vector and under the knockdown of E2F1 in PC3 and DU145 cells by RNA sequencing (RNA-seq). To investigate differentially expressed genes (false discovery rate (FDR) <0.05, |log2 (Fold Change)| > 1) between vector control and shE2F1 of CRPC cells, we performed processing RNA-Seq data using the Basespace. Then we verified some common two cells’ differentially expressed genes through quantitative real-time PCR.

2019-10-18 | GSE121258 | GEO

Expression data from Docetaxel-resistant prostate cancer cells

Project description:Docetaxel is the standard first line therapy for hormone-refractory prostate cancer patients. Here we generated models of Docetaxel resistance in prostate cancer cells to study the molecular pathways that drive the acquisition of resistance to this therapy. We used microarrays to detail the global program of gene expression underlying the acquisition of Docetaxel resistance in prostate cancer cells. Parental Docetaxel-sensitive prostate cancer cell lines (DU145 and 22Rv1) and selected Docetaxel-resistant cells (DU145-DR and 22Rv1-DR) were harvested for RNA extraction and hybridization on Affymetrix microarrays. Samples were analyzed in triplicates in order to increase the resolution of expression profiles.

2012-10-02 | E-GEOD-36135 | 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