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RNA Sequencing of 16D Prostate Cancer Cell Lines with genetic knockout and rescue of OGDHL

ABSTRACT: The goal of this study was to perform transcriptomics of prostate cancer cells with genetic knockout and rescue of OGDHL treated with the Androgen Receptor Pathway Inhibitor Enzalutamide (Enza) or Vehicle (DMSO)

ORGANISM(S): Homo sapiens

PROVIDER: GSE315048 | GEO | 2025/12/30

REPOSITORIES: GEO

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RNA Sequencing of 16D Prostate Cancer Cell Lines with genetic knockout of OGDHL

Project description:The goal of this study was to perform transcriptomics of prostate cancer cells with genetic knockout of OGDHL treated with the Androgen Receptor Pathway Inhibitor Enzalutamide (Enza) or Vehicle (DMSO)

2025-06-06 | GSE298123 | GEO

Chromatin Occupancy of AR, BRD4, and H3K27Ac in MR42D Cells in response to Enzalutamide [RNA-seq]

Project description:To identify mechanisms that contribute to lineage plasticity and t-NEPC, we focused on enza-resistant cell lines with persistent AR expression that have features of lineage plasticity, including high expression of NEPC markers: the MR42D and MR42F cell lines. We cultured these enzalutamide resistant lines, which are usually maintained in medium with enzalutamide, without enzalutamide for 72 hors to "washout" the effects of enzalutamide, and then either enzalutamide or vehicle was added back to the growing media for 24 hours. Enzalutamide sensitive lines LNCaP and V16D were treated with either enzalutamide or vehicle for 24 hours. Enzalutamide reversibly increased expression neuronal markers in MR42D and MR42F cells, but not enza-sentitive LNCaP and V16D cells, suggesting that the AR may negatively regulate neuronal gene expression in these t-NEPC cells. Moreover, bromodomain inhibitors (BETi) ARV-771 and JQ1 reduced expression of NEPC target genes in MR42D cells.

2021-06-22 | GSE147876 | GEO

RNA sequencing of 16D CRPC cells treated with enzalutamide over varying periods of time

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2022-05-12 | GSE202885 | GEO

RNA sequencing of 16D LTenza cells transduced with cMyc, shRb1, shTp53, shRb1_shTp53

Project description:The goal of this study was to determine how genetic alterations to AR inhibition-maintained prostate cancer cells alters transcriptional programs. We explored how MYC overexpression alters the transcriptional program of 16D cells maintained in enzalutamide for at least 2 months (LTenza) by transducing LTenza 16D cells with control (FUCRW) or MYC. To explore the effect of RB1 and TP53, we generated LTenza 16D cells with knockdown of RB1 and/or TP53 and compared these lines to control-transduced (shScr) LTenza 16D cells. Enzalutamide-naïve (DMSO-treated) cells were included to validate enzalutamide-induced inhibition of AR signaling in enzalutamide-maintained lines.

2022-05-12 | GSE202897 | GEO

Chromatin Occupancy of AR, BRD4, and H3K27Ac in MR42D Cells in response to Enzalutamide [ChIP-seq]

Project description:In order to identify AR-repressed genes that are activated by enzalutamide in t-NEPC cell lines, we cultured enza-resistant MR42D cells in the absence of enzalutamide for 72 hours, then added back either enzalutamide or vehicle and cultured for an additional 24 hours. Then we performed chromatin immunoprecipitation sequencing (ChIP-seq) pulling down AR, BRD4, and H3K27Ac. To identify potential NEPC genes suppressed by the AR, we compared AR DNA occupancy from the vehicle and enzalutamide treatments to identify regions where AR was evicted in response to enzalutamide. Similarly to determine the role of histone acetylation on NEPC gene activation in t-NEPC lines, we examined differential DNA-binding of the BRD4 acetylated lysine reader, and differential acetylation of the active enhancer mark H3K27Ac in response to enzalutamide treatment.

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Identification of Radiosensitivity Gene Signatures Induced by Enzalutamide in Prostate cancer cells

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Project description:Analysis of enzalutamide- and/or olaparib-responsive gene expression in prostate cancer cells. The hypothesis tested in the present study was that enzalutamide influences the expression of genes that are involved in important bioprocesses in prostate cance rcells, including DNA damage response genes and this effect may synergize with poly(ADP-ribose) polymerase inhibitor olaparib in cytotoxicity to prstate cancer cells. prostate cancer cells were pretreated with enzalutamide or vehicle control DMSO for 24 h, followed by treatment with enzalutamide, olaparib, enzalutamide+olaparib, or vehicle control DMSO for 48 h. Gene expression in enzalutamide+olaparib-treated cells was compared with taht in vehicle control- and single agent-treated cells.

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Identification of drivers and therapeutic vulnerabilities in anti-androgen resistant prostate cancer cells

Project description:Inhibition of the androgen receptor (AR) by anti-androgens is the standard treatment for castration resistant prostate cancer (CRPC), but it inevitably leads to the development of resistance. We generated two multi anti-androgen resistant cell-line models by treatment of LNCaP cells with enzalutamide (ResA) and RD-162 (ResB). Both cell-lines have an AR independent, non-neuroendocrine phenotype. To identify the resistance mechanisms we performed RNASeq analysis. To this end, the three cell-lines were plated in medium with 5% dextran-coated charcoal (DCC) treated FCS at a density of 1 million cells/well in 6-well plates. After 24 hours of steroid starvation the cells were treated with 10 nM of the androgen dihydrotestosterone (DHT), 10 µM of the anti-androgen enzalutamide, a combination of the two, or vehicle (DMSO) for 18 hours.

2019-09-26 | GSE130534 | GEO

Proteome profiling of enzalutamide-resistant cell lines and serum analysis identified ALCAM as marker of resistance in castration-resistant prostate cancer

Project description:Enzalutamide (ENZA) is a frequently used therapy in metastatic castration-resistant prostate cancer (mCRPC). Baseline or acquired resistance to ENZA have been observed, but the molecular mechanisms of resistance are poorly understood. We aimed to identify proteins involved in ENZA resistance and to find therapy-predictive serum markers. We performed comparative proteome analyses on ENZA-sensitive parental (LAPC4, DUCAP) and -resistant prostate cancer cell lines (LAPC4-ENZA, DUCAP-ENZA) using liquid chromatography tandem mass spectrometry (LC-MS/MS). The most promising 4 marker candidates were selected using bioinformatic approaches. Serum concentrations of selected markers (ALCAM, AGR2, NDRG1, IDH1) were measured in 72 ENZA-treated mCRPC patients’ samples using ELISA. In addition, ALCAM serum levels were measured in 101 Abiraterone (ABI) and 100 Docetaxel (DOC)-treated mCRPC patients. Results were correlated with clinical and follow-up data. The functional role of ALCAM in ENZA resistance was assessed in vitro using siRNA. Our proteome analyses revealed 731 significantly differentially abundant proteins between ENZA-sensitive and -resistant cells and our filtering methods identified 4 biomarker candidates. Serum analyses of these proteins revealed only ALCAM to be associated with poor patient survival. Furthermore, higher baseline ALCAM levels were associated with poor survival in ABI- but not in DOC-treated patients. In LAPC4-ENZA resistant cells, ALCAM silencing by siRNA knockdown resulted in significantly enhanced ENZA sensitivity. Our analyses revealed that ALCAM serum levels may help to identify ENZA- and ABI-resistant patients and may thereby help to optimize future clinical decision-making. Our functional analyses suggest the possible involvement of ALCAM in ENZA resistance.

2022-06-24 | PXD031847 | Pride

RNA-seq analysis regarding antiandrogen (enzalutamide) effect on gene expression in castration-resistant prostate cancer (CRPC) xenograft model

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2022-05-02 | GSE147541 | GEO

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