RNA Sequencing of 16D Prostate Cancer Cell Lines with genetic knockdown of OGDHL
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE298311 | GEO | 2026/03/31
REPOSITORIES: GEO
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Project description: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)
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Project description:To investigate the mechanisms of drug resistance and castration resistance in prostate cancer, we performed proteomic sequencing on androgen-dependent prostate cancer cells (LNCaP) and androgen-independent cells (AI) treated with enzalutamide.
2024-11-26 | PXD058261 |
Project description:The goal of this study was to determine how androgen receptor inhibition alters transcriptional programs in castration-resistant prostate cancer cells. 16D castration-resistant prostate cancer cells were grown in the presence of 10 micromolar enzalutamide for 24, 48, 96, 144 hours or for more than 2 months (long-term). Analysis shows that androgen receptor target genes are reduced with enzalutamide while metabolic genes are also differentially expressed.
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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
Project description:The goal of this study was to perform transcriptomics of xenograft tumors generated from prostate cancer cells with genetic knockout of OGDHL vs a control knockout
2025-06-06 | GSE297510 | GEO
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
Project description:Background. Androgen receptor splice variant-7 (AR-V7) is a truncated form of the androgen receptor protein which lacks the ligand-binding domain, the target of enzalutamide and abiraterone, but remains constitutively active as a transcription factor. We hypothesized that detection of AR-V7 in circulating tumor cells (CTCs) from men with advanced prostate cancer would be associated with resistance to enzalutamide and abiraterone. Methods. We used quantitative reverse-transcription polymerase-chain-reaction (qRT-PCR) to interrogate CTCs for the presence or absence of AR-V7 from prospectively enrolled patients with metastatic castration-resistant prostate cancer initiating treatment with either enzalutamide or abiraterone. We examined associations between AR-V7 status and PSA response rates, PSA-progression-free-survival (PSA-PFS), clinical/radiographic-progression-free-survival (PFS), and overall survival (OS). Multivariable Cox regression analyses were performed to determine the independent effect of AR-V7 status on clinical outcomes. Results. Thirty-one enzalutamide-treated patients and thirty-one abiraterone-treated patients were enrolled, of which 38.7% and 19.4% had detectable AR-V7 from CTCs, respectively. Among men receiving enzalutamide, AR-V7–positive patients had inferior PSA response rates (0% vs 52.6%, P=0.004), PSA-PFS (median: 1.4 vs 6.0 months, P<0.001), PFS (median: 2.1 vs 6.1 months, P<0.001), and OS (median: 5.5 months vs not reached, P=0.002) compared to AR-V7–negative patients. Similarly, among men receiving abiraterone, AR-V7–positive patients had inferior PSA response rates (0% vs 68.0%, P=0.004), PSA-PFS (median: 1.3 months vs not reached, P<0.001), PFS (median: 2.3 months vs not reached, P<0.001), and OS (median: 10.6 months vs not reached, P=0.006). The negative prognostic impact of AR-V7 was maintained after adjusting for full-length-AR expression. Conclusions. Detection of AR-V7 in CTCs from patients with castration-resistant prostate cancer is associated with resistance to enzalutamide and abiraterone. A total of four metastatic castration-resistant prostate tumor samples from four patients were subjected to RNA-seq. Two samples were positive for androgen receptor splice variant 7 and the other two were negative for this variant.
2014-09-03 | E-GEOD-56701 | biostudies-arrayexpress
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
Project description:Enzalutamide, a second-generation androgen receptor (AR) antagonist, has demonstrated clinical benefit in men with prostate cancer. However, it only provides a temporary response and modest increase in survival, indicating a rapid evolution of resistance. Previous studies suggest that enzalutamide may function as a partial transcriptional agonist, but the underlying mechanisms for enzalutamide-induced transcription remain poorly understood. Here, we show that enzalutamide stimulates expression of a novel subset of genes distinct from androgen-responsive genes. Treatment of prostate cancer cells with enzalutamide enhances recruitment of pioneer factor GATA2, AR, Mediator subunits MED1 and MED14, and RNA Pol II to regulatory elements of enzalutamide-responsive genes. Mechanistically, GATA2 functions in directing AR, Mediator and Pol II loading to enzalutamide-responsive gene loci. Importantly, the GATA2 inhibitor K7174 inhibits enzalutamide-induced transcription by decreasing binding of the GATA2/AR/Mediator/Pol II transcriptional complex, contributing to sensitization of prostate cancer cells to enzalutamide treatment. Our findings provide mechanistic insight into the future combination of GATA2 inhibitors and enzalutamide for improved AR-targeted therapy.
2019-09-03 | GSE125014 | GEO