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Effect of MPC309 (AR-targeting Multivalent Peptoid Conjugate) treatment on gene expression in LNCaP-ABL cells (castration-resistant prostate cancer cell line) in comparison to Vehicle control and another AR ligand, Ethisterone (partial agonist): RNA-Seq

ABSTRACT: Effect of MPC309 (AR-targeting Multivalent Peptoid Conjugate) treatment on gene expression in LNCaP-ABL cells (castration-resistant prostate cancer cell line) in comparison to Vehicle control and another AR ligand, Ethisterone (partial agonist): RNA-Seq

PROVIDER: PRJNA989627 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25099378_1.fastq.gz	Fastqsanger.gz
	SRR25099378_2.fastq.gz	Fastqsanger.gz
	SRR25099379_1.fastq.gz	Fastqsanger.gz
	SRR25099379_2.fastq.gz	Fastqsanger.gz
	SRR25099380_1.fastq.gz	Fastqsanger.gz

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Effect of MPC309 (AR-targeting Multivalent Peptoid Conjugate) treatment on gene expression in LNCaP-ABL cells (castration-resistant prostate cancer cell line) in comparison to Vehicle control and another well-known AR ligand, Ethisterone (partial agonist)

Project description:Effect of MPC309 (an AR-targeting Multivalent Peptoid Conjugate) treatment on gene expression in LNCaP-ABL cells (a castration-resistant prostate cancer cell line) in comparison to Vehicle control and another well-known AR ligand, Ethisterone (partial agonist). Prostate cancers adapt to androgen receptor (AR) pathway inhibitors and progress to castration resistance due to ongoing AR expression and function. To counter this, we developed a new approach to modulate the AR and inhibit castration-resistant prostate cancer (CRPC) using multivalent peptoid conjugates (MPCs) that contain multiple copies of the AR-targeting ligand ethisterone attached to a peptidomimetic scaffold. To determine if the effects of MPC309 differ from those of ethisterone alone, we conducted RNA-seq analysis on LNCaP-abl cells. These cells were treated overnight with either a control vehicle (DMSO), MPC309, or ethisterone. Our analysis revealed that there was minimal overlap in the genes regulated by MPC309 and ethisterone alone.

2023-07-11 | GSE236088 | GEO

Project description:Prostate cancers evolve to resist androgen receptor (AR) pathway inhibitors, such as enzalutamide, leading to castration resistance due to sustained AR expression and function. In response, we have designed a novel strategy to regulate the AR and suppress castration-resistant prostate cancer (CRPC) by employing multivalent peptoid conjugates (MPCs). These conjugates comprise multiple copies of the AR-targeting ligand ethisterone attached to a peptidomimetic framework. To pinpoint the genes and pathways impacted by MPC309, we performed RNA-sequencing on LNCaP-abl cells, which were treated overnight with various agents: vehicle (DMSO), peptoid backbone, MPC309, dihydrotestosterone (an AR activator), or enzalutamide (an AR inhibitor commonly used clinically). Our findings revealed unique gene expression patterns (transcriptomes) in cells exposed to each compound, indicating that MPC309 may be a new AR ligand influencing the AR transcriptional response.

2023-07-11 | GSE236286 | GEO

Expression data of treated LNCaP-abl cells

Project description:We introduce a family of multivalent peptidomimetic conjugates that modulate the activity of the androgen receptor (AR). Bioactive ethisterone ligands were conjugated to a set of sequence-specific peptoid oligomers. Certain multivalent peptoid conjugates enhance AR-mediated transcriptional activation. We identify a linear and a cyclic conjugate that exhibit potent anti-proliferative activity in LNCaP-abl cells, a model of therapy-resistant prostate cancer. The linear conjugate blocks AR action by competing for ligand binding. In contrast, the cyclic conjugate is active despite its inability to compete against endogenous ligand for binding to AR in vitro, suggesting a non-competitive mode of action. These results establish a versatile platform to design competitive and non-competitive AR modulators with potential therapeutic significance. We use microarray analysis to further elucidate the mechanism of AR antagonism and show that the compounds (cyc and n=8) are distinct. We used microarray analysis to see genone-wide effects on LNCaP-abl cells with moduators of AR activity LNCaP-abl cells were treated with compound and RNA was extracted and hybridized on Affymetrix microarrays Treatments: Vehicle is just Ethanol treated LNCaP-abl cells that were used as a control. n=8 and cyc are peptoid conjugates that modulate AR activity. n=8 is linear and cyc is a cyclic compounds. We wanted to look at gene expression when LNCaP-abl cells were treated with these compounds to show that they are distinct. C3 is a small molecule that inhibits the interaction between AR and beta-catenin (co-regulator protein). Initial results with this compound show potent anti-proliferative activity in LNCaP-abl cells and we wanted to further investigate the mechanism of action of this compound.

2012-12-21 | E-GEOD-37796 | biostudies-arrayexpress

Expression data of treated LNCaP-abl cells

2012-12-21 | GSE37796 | GEO

Project description:To establish wehther the genes stimulated or inhibited by MPC309 are directly influenced by the AR, we conducted ChIP-seq of AR from LNCaP-abl cells that had been treated with vehicle (DMSO), MPC309, Backbone, DHT, or Enzalutamide overnight. Our results revealed a more pronounced AR presence in cells exposed to MPC309 and DHT as compared to control groups and those treated with enzalutamide, reinforcing the idea that MPC309 facilitates distinct AR interactions with chromatin. Genes linked with AR occupancy mirrored similar GO terms as those seen in RNA-seq experiments. Out of the 251 genes repressed by MPC309 compared to controls (vehicle and backbone), 246 (98%) had an AR binding site within 15 kb upstream or downstream of the gene promoter. Similarly, of the 405 genes stimulated by MPC309, 387 (96%) had an AR binding site within 15 kb of the gene promoter. These observations suggest that the gene regulation driven by MPC309 stems from AR interactions with chromatin, resulting in varying impacts on gene expression compared to DHT or enzalutamide, consequently inhibiting the growth of prostate cancer cells.

2023-07-11 | GSE236287 | GEO

Project description:We conducted ATAC-seq on LNCaP-abl cells treated overnight with either vehicle (DMSO), MPC309, Backbone, DHT or Enzalutamide to reveal areas of accessible chromatin. Our results indicated that the vast majority of peaks (>46,000) were shared among all groups. Notwithstanding, MPC309 incited some chromatin restructuring, as evidenced by the unique 8,750 open chromatin sites seen in cells treated with MPC309 as opposed to those treated with the vehicle. Analysis of transcription factor (TF) binding-motifs around regions of chromatin exclusively open in MPC309-treated cells exposed NR-binding motifs (GRE, PRE, ARE, AR-half sites). This indicates the potential for MPC309-bound AR to interact with chromatin at AR-specific locations.

2023-07-11 | GSE236288 | GEO

Project description:Effect of MPC309 (AR-targeting Multivalent Peptoid Conjugate) treatment on gene expression in LNCaP-ABL cells (castration-resistant prostate cancer cell line) in comparison to Vehicle control and another well-known AR ligand, Ethisterone (partial agonist)

| PRJNA988814 | ENA

| PRJNA989628 | ENA

| PRJNA989629 | ENA

Effects of Cardiac Glycosides on RNA Expression in Prostate Cancer LNCaP-abl Cells

Project description:Prostate cancer is the most common cancer in men and cardiac glycosides inhibit prostate cancer cell proliferation. In order to investigate the mechanism by which cardiac glycosides inhibit prostate cancer cells, we observed genome-wide RNA expression in prostate cancer LNCaP-abl cells, hormone resistant cells, after the cardiac glycoside treatment using RNA-Seq. In addition, we profiled LNCaP-abl cells after androgen receptor (AR) knockdown to observe whether cardiac glycoside effect on RNA expression is similar to that of AR knockdown. Observation of three cardioglycosides, Digoxin, Peruvoside and Strophanthidin, and AR knockdown regulated RNA expression in LNCaP-abl with RNA-Seq (each triplicates)

2012-04-03 | E-GEOD-35126 | biostudies-arrayexpress

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