Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RUVBL1 promotes enzalutamide resistance of prostate tumors through the PLXNA1-CRAF-MAPK pathway

ABSTRACT: RUVBL1 promotes enzalutamide resistance of prostate tumors through the PLXNA1-CRAF-MAPK pathway

PROVIDER: PRJNA812051 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

RUVBL1 promotes enzalutamide resistance of prostate tumors through the PLXNA1-CRAF-MAPK pathway

Project description:RUVBL1 promotes enzalutamide resistance of prostate tumors through the PLXNA1-CRAF-MAPK pathway

| PRJNA811241 | ENA

RUVBL1 promotes enzalutamide resistance of prostate tumors through the PLXNA1-CRAF-MAPK pathway

Project description:The aim of this research was to confirm the regulatory effect of RUVBL1 on gene expression in castration resistant prostate cancer.

2022-03-02 | GSE197630 | GEO

Ligand-independent CXCR7 Activation of MAPK Signaling leads to Prostate Cancer Enzalutamide Resistance

Project description:The standard of care for patients with advanced form of prostate cancer, castration-resistant, now includes enzalutamide, a second generation antiandrogen. However, most of the treated patients will develop resistance to enzalutamide based therapy in around a year, succumbing to lethal disease. Investigating the transcriptome of enzalutamide-resistant prostate cancer cell lines, we identified CXCR7 as one of the most upregulated genes suggesting its role in advanced prostate cancer. CXCR7, known as an atypical G-coupled receptor, is engaged in many physiological and pathological processes. Here we show that in prostate cancer CXCR7 is tightly regulated by androgen receptor (AR), which directly binds to CXCR7 gene promoter and enhancer and represses its transcription. In turn, CXCR7 in prostate cancer reduces enzalutamide toxicity and promotes cell survival and invasiveness. We identified that CXCR7 forms an integral complex with ARRB2 and activates ERK1/2, eliciting pro-survival MAPK pathway. Enzalutamide treatment combined with MAPKK specific inhibitor, trametinib, reversed enzalutamide resistance in prostate cancer in vitro and in vivo. Taken together our findings highlight the critical role of CXCR7 in enzalutamide-resistant prostate cancer and open an avenue for developing novel anti-CXCR7 therapies to improve survival in patients with advanced prostate cancer.

2019-04-06 | GSE104935 | GEO

Ligand-independent CXCR7 Activation of MAPK Signaling leads to Prostate Cancer Enzalutamide Resistance

Project description:Ligand-independent CXCR7 Activation of MAPK Signaling leads to Prostate Cancer Enzalutamide Resistance

| PRJNA414193 | ENA

Targeting DNMTs to overcome enzalutamide resistance in prostate cancer

Project description:Prostate cancer is the second leading cause of cancer death among men in the United States. The androgen receptor (AR) antagonist enzalutamide is a FDA-approved drug for treatment of patients with late-stage prostate cancer and is currently under clinical study for early-stage prostate cancer treatment. After a short positive response period to enzalutamide, tumors will develop drug resistance. In this study, we uncovered that DNA methylation was deregulated in enzalutamide-resistant cells. DNMT activity and DNMT3B expression were upregulated in resistant cell lines. Enzalutamide induced the expression of DNMT3A and DNMT3B in prostate cancer cells with a potential role of p53 and pRB in this process. The overexpression of DNMT3B3, a DNMT3B variant, promoted an enzalutamide-resistant phenotype in C4-2B cell lines. Inhibition of DNA methylation and DNMT3B knockdown induced a re-sensitization to enzalutamide. Decitabine treatment in enzalutamide-resistant cells induced a decrease of the expression of AR-V7 and changes of genes for apoptosis, DNA repair and mRNA splicing. Combination treatment of Decitabine and enzalutamide induced a decrease of tumor weight, Ki-67 and AR-V7 expression and an increase of cleaved-caspase3 levels in 22Rv1 xenografts. The collective results suggest that DNA methylation pathway is deregulated after enzalutamide resistance onset and that targeting DNA methyltransferases restores the sensitivity to enzalutamide in prostate cancer cells.

2021-09-22 | GSE184168 | GEO

Acquired Resistance to the Second-Generation Androgen Receptor Antagonist Enzalutamide in Castration-Resistant Prostate Cancer

Project description:Illumina gene array analyses of prostate cancer cell lines that had acquired resistance to Enzalutamide (MDV3100). mRNA analyses of four cell lines (CWR-R1, LAPC-4, LNCaP, and VCAP) cells that were either untreated, treated for 48hrs with Enz (short-term), or continuously grown in Enzalutamide for >6 months.

2016-02-24 | E-GEOD-78201 | biostudies-arrayexpress

Enzalutamide resistance in prostate cancer cells

Project description:Enzalutamide resistance in prostate cancer cells

| PRJNA633640 | ENA

Expression data from prostate cancer cell lines C4-2B (enzalutamide sensitive) and C4-2B-MDVR (enzalutamide resistant) cells

Project description:Prostate cancer C4-2B cells were cultured in enzalutamide in a dose-escalation manner. After sixty passages cells were resistant to enzalutamide, with a specific sets of genes been deregulated. We performed global gene expression analysis by cDNA microarrays to identify genes responsible for enzalutamide resistance in C4-2B-MDVR cells. Enzalutamide resistant C4-2B-MDVR cells were selected from C4-2B cells during long time enzalutamide treatment. Genes responsible for enzalutamide resistance were identified using C4-2B vs. C4-2B-MDVR RNA extraction and hybridization on Affymetrix microarrays.

2015-04-09 | E-GEOD-64143 | biostudies-arrayexpress

Enzalutamide resistance in prostate cancer cells

Project description:Castration resistant prostate cancer (CRPC) develops resistance to antiandrogens affecting Androgen Receptor (AR) signaling through a variety of mechanism. Because of this, the efficacy of androgen receptor targeted therapy remains limited for many patients with CRPC. We developed LNCaP-enzalutamide (ENZU) and resistance cells to study changes in transcriptomic profile compared to parental cells.

2020-12-31 | GSE150807 | GEO

NOTCH signaling is activated in and contributes to resistance in enzalutamide-resistant prostate cancer cells

Project description:Prostate cancer is the second leading cause of cancer death among men in the United States. The Androgen receptor (AR) antagonist Enzalutamide is a FDA approved therapy for treatment of late stage prostate cancer patients and is currently under clinical study for early stage prostate cancer treatment. After a short positive response period, patients will develop drug resistance. In this study we used RNA-sequencing and bioinformatics analysis to identify Notch signaling pathway as a deregulated pathway in Enzalutamide-resistant cells. NOTCH2 and c-MYC positively correlated with AR expression in patients' samples mimicking cells with Enzalutamide-resistance. In Enzalutamide-resistant cells, MR49F and C4-2R, we found that cleaved-NOTCH1, HES1 and c-MYC protein expression are significantly elevated indicating an activated NOTCH1 pathway in those cells. In addition, ADAM10 and ADAM17 had a higher expression in Enzalutamide-resistant cells, suggesting a role for S2 cleavage in the increased cleaved NOTCH1 expression. Furthermore, treatment of Enzalutamide-resistant cells with PF-03084014 in combination with Enzalutamide increased cell death, decreased colony formation ability and re-sensitized Enzalutamide-resistant cells to Enzalutamide. Knockdown of NOTCH1 in C4-2R increases Enzalutamide sensitivity by decreasing cell proliferation and increasing cell death. In a 22RV1 xenograft model, PF-03084014 and Enzalutamide induced a decrease in tumor growth through a reduced cell proliferation and increased apoptosis. These results indicate that Notch1 signaling can contribute to Enzalutamide-resistance in Prostate cancer and inhibition of this pathway can re-sensitize resistant cells to Enzalutamide.

2019-04-01 | GSE123379 | GEO

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