Project description:Transriptome analysis of VCAP and CWR22-Pc cell lines after concomittant treatment with androgen with bicalutamide and enzalutamide
Project description:Prostate cancer patients benefit from treatment with androgen receptor signaling inhibitors such as AR antagonists. The emergence of resistance to the clinically applied AR antagonists opens up the need for development of alternative AR antagonists. We show here the development of a novel AR antagonists that is structurally different from enzalutamide. Moreover, MEL-6 remains active in the presence of several AR mutations (T877A, W741C and F876L) that are found in patients resistant to hydroxyflutamide, bicalutamide and enzalutamide. To validate the androgen receptor (AR) as the target of our experimental AR antagonist, MEL-6, we investigated the effect of MEL-6 treatment on the prostate cancer cell line, LNCaP.
Project description:Transriptome analysis of prostate tumors from Hi-Myc mouse prostates 3 days after castration or treatment with bicalutamide or enzalutamide
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.
Project description:Gene expression in LNCaP cells after treatment with the androgen receptor targeting drugs bicalutamide (BIC), enzalutamide (ENZ) and apalutamide (ARN) in the presence or absence of dihydrotestosterone (DHT).
Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. To investigate the AR signaling, we performed CaP analysis of gene expression (CAGE) analysis in AR positive prostate cancer cell line, LNCaP. In addition, we used hormone-refractory prostate cancer model cells, Bicalutamide-resistant (BicR) to explore the differences of androgen signaling in prostate cancer progression. CAGE analysis of androgen-regulated transcripts in two prostate cancer cells
Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. To investigate the AR signaling, we performed RNA sequence analysis in AR positive prostate cancer cell line, LNCaP. In addition, we used hormone-refractory prostate cancer model cells, Bicalutamide-resistant (BicR) to explore the differences of androgen signaling in prostate cancer progression. Short RNA sequence analysis of androgen-regulated miRNAs in two prostate cancer cells
Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. To investigate the AR signaling, we performed short RNA sequence analysis in AR positive prostate cancer cell line, LNCaP. In addition, we used hormone-refractory prostate cancer model cells, Bicalutamide-resistant (BicR) to explore the differences of androgen signaling in prostate cancer progression. Short RNA sequence analysis of androgen-regulated miRNAs in two prostate cancer cells
Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. To investigate the AR signaling, we performed ChIP sequence analysis in AR positive prostate cancer cell line, LNCaP. In addition, we used hormone-refractory prostate cancer model cells, Bicalutamide-resistant (BicR) to explore the differences of androgen signaling in prostate cancer progression.
