Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression analysis of C4-2 cells treated with ACLY inhibitor and Enzalutamide

ABSTRACT: This study examined the gene expression effects of treating androgen-deprived C4-2 prostate cancer cells with the ACLY inhibitor BMS-303141 and the AR antagonist enzalutamide.

ORGANISM(S): Homo sapiens

PROVIDER: GSE81796 | GEO | 2017/02/10

SECONDARY ACCESSION(S): PRJNA322550

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

High-throughput profiling of mRNA from parental and Enzalutamide resistant C4-2b prostate cancer cell lines

Project description:We established an enzalutamide-resistant C4-2b prostate cell line that has an active androgen receptor by maintaining the C4-2b cell line in serially increasing concentrations of enzalutamide. Among the CRPC cell lines, we selected the C4-2b cell line because it is known to have AR variants, and we desired to identify enzymes with the ability to regulate the activity of AR variants as well as the wild type AR. After 2 months, we acquired resistant cells in even 10 uM enzalutamide. After validation of enzalutamide-resistant character, we analyzed global changes in mRNA expression by using quantitative mRNA-sequencing analysis.

2020-02-01 | GSE110802 | GEO

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

2015-04-09 | GSE64143 | GEO

Transcriptome analysis of enzalutamide-sensitive and -resistant C4-2B cells

Project description:The overall goal of this study was to identify genes differentially expressed in enzalutamide-sensitive (C4-2B Con) and enzalutamide-resistant (C4-2B ENZR) C4-2B cells.

2020-10-20 | GSE159548 | GEO

Transcriptome analysis of effects of AHR knockdown in Enzalutamide-resistant CWR-R1 and C4-2B cells

Project description:Enzalutamide (ENZ) is an inhibitor of the androgen receptor (AR) widely used in managing castration-resistant prostate cancer (CRPC). AHR was found upregulated in different Enzalutamide-resistant (ENZR) prostate cancer cell lines. Knocking down AHR significantly decreased the growth of CWR-R1ENZR and C4-2BENZR cells. To elucidate the underlying mechanism of AHR-mediated growth, we transcriptionally profiled CWR-R1ENZR and C4-2BENZR cells stably expressing control and two AHR-targeting shRNAs. AHR maintained androgen response in CWR-R1ENZR cells likely through driving the expression of many genes targeted by both the androgen receptor and glucocorticoid receptor. Interestingly, knockding down AHR did not have the same effect in C4-2BENZR cells. Instead of strengthing AR signaling, AHR maintained features of neuroendocrine differentiation, an AR-independent mechanism of ENZ resistance, in C4-2BENZR cells. Our results supported that AHR regulates transcriptional networks promoting ENZ resistance in a lineage-dependent manner and holds great potential as a therapeutic target.

2026-02-28 | GSE289910 | GEO

RNA-seq of C4-2 parental and enzalutamide resistant cells

Project description:To explore the potential drug target candidate in enzalutamide-resistant PCa, the differential abundances of transcripts between enzalutamide-resistant C4-2 Enz-R and C4-2 cells were examined.

2025-01-14 | GSE285929 | GEO

FMNL2/SRC-mediated androgen receptor translocation into the nucleus promotes enzalutamide resistance of prostate cancer

Project description:Enzalutamide, a second-generation androgen receptor (AR) antagonist, has represented the association with improved overall survival in men with prostate cancer (PCa). However, PCa patients receiving enzalutamide will eventually develop resistance through various mechanisms without effective regimens. Here, we observed a higher level of formin-like 2 (FMNL2) in enzalutamide-resistant PCa cells. Functionally, FMNL2 knockdown partially re-sensitized enzalutamide-resistant PCa cells. Mechanistically, FMNL2 directly interacted with SRC kinase through FMNL2-FH1 and SRC-SH3 domain, which induced AR translocation from the cytoplasm to the nucleus, resulting in increased expression of the AR-targeted genes and leading to resistance to enzalutamide. Consistently, SRC inhibitor dasatinib rescued enzalutamide sensitivity and inhibited the proliferation of enzalutamide-resistant cancer cells. Taken together, our findings demonstrate a substantial role for FMNL2/SRC interaction in the regulation of AR translocation, suggesting that targeting FMNL2-mediated SRC activation might be a potential therapeutic strategy for enzalutamide-resistant PCa, and dasatinib could be an option.

2025-01-13 | PXD059539 | Pride

Transcriptomic profiling of LNCaP/C4-2 cells under stepwise androgen receptor inhibition

Project description:This study presents transcriptomic profiling of human prostate cancer cell lines under stepwise androgen receptor (AR) inhibition. LNCaP and C4-2 cells were cultured under untreated conditions, androgen deprivation using charcoal-stripped serum, long-term exposure to the first-generation AR antagonist bicalutamide, or long-term exposure to the second-generation AR antagonist enzalutamide. Drug-resistant cell populations were generated through gradual dose escalation. The neuroendocrine prostate cancer cell line NCI-H660 was included as a reference. Bulk RNA sequencing was performed for three biological replicates per condition. The dataset provides a resource for investigating transcriptional responses to progressive AR suppression and adaptive changes associated with AR-targeted therapies.

2026-01-07 | GSE315550 | GEO

Cellular androgen content influences enzalutamide agonism of F877L mutant androgen receptor

Project description:Prostate cancer is the most commonly diagnosed and second-most lethal cancer among men in the United States. The vast majority of prostate cancer deaths are due to castration-resistant prostate cancer (CRPC) â?? the lethal form of the disease that has progressed despite therapies that interfere with activation of androgen receptor (AR) signaling. One emergent resistance mechanism to medical castration is synthesis of intratumoral androgens that activate the AR. This insight led to the development of the AR antagonist enzalutamide. However, resistance to enzalutamide invariably develops, and disease progression is nearly universal. One mechanism of resistance to enzalutamide is an F877L mutation in the AR ligand-binding domain that can convert enzalutamide to an agonist of AR activity. However, mechanisms that contribute to the agonist switch had not been fully clarified, and there were no therapies to block AR F877L. Using cell line models of castration-resistant prostate cancer (CRPC), we determined that cellular androgen content influences enzalutamide agonism of mutant F877L AR. Further, enzalutamide treatment of AR F877L-expressing cell lines recapitulated the effects of androgen activation of F877L AR or wild-type AR. Because the BET bromodomain inhibitor JQ-1 was previously shown to block androgen activation of wild-type AR, we tested JQ-1 in AR F877L-expressing CRPC models. We determined that JQ-1 suppressed androgen or enzalutamide activation of mutant F877L AR and suppressed growth of mutant F877L AR CRPC tumors in vivo, demonstrating a new strategy to treat tumors harboring this mutation. RNA-seq profiles of prostate cancer cell lines to understand gene expression associated with enzalutamide treatment

2016-06-10 | E-GEOD-69896 | biostudies-arrayexpress

Transcriptome analysis of Enzalutamide-sensitive and -resistant CWR-R1, C4-2B, and VCaP cells

Project description:Enzalutamide (ENZ) is an inhibitor of the androgen receptor (AR) widely used in managing castration-resistant prostate cancer (CRPC). However, ENZ is not curative due to the resistance CRPC inevitably develops. We hypothesize that there are commonly necessary elements of ENZ resistance in cells with different genetic mutations and treatment history. This study aims to identify differentially expressed genes in Enzalutamide-sensitive (ENZS) and ENZ-resistant (ENZR) C4-2B, CWR-R1, VCaP human prostate cell lines. We have identified 114 commonly upregulated genes in all three ENZR celll lines, which will be subjected to further investigation for their roles in ENZ resistance.

2026-02-28 | GSE290016 | 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