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The effect of MEL-6 on gene expression in LNCaP cells

ABSTRACT: The effect of MEL-6 on gene expression in LNCaP cells

PROVIDER: PRJNA1017839 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26071664.fastq.gz	Fastqsanger.gz
	SRR26071665.fastq.gz	Fastqsanger.gz
	SRR26071666.fastq.gz	Fastqsanger.gz
	SRR26071667.fastq.gz	Fastqsanger.gz
	SRR26071668.fastq.gz	Fastqsanger.gz

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The effect of MEL-6 on gene expression in LNCaP cells

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.

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Effect of KHSRP acetylation on gene expression in LNCaP cells

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Effect of KHSRP acetylation on gene expression in LNCaP cells

Project description:We established LNCaP cells in wihch KHSRP was knocked down along with LNCaP cells with silenced KHSRP and re-introduced HA-tagged KHSRP-WT/K205R.RNA-seq was carried out in the stable LNCaP cell lines to determine the underlying mechanism of KHSRP acetylation in PCa tumorigenesis. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different cells.

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Project description:LINC01518 is differentially expressed in prostate cancer, but the exact role and potential mechanisms are unknown. We overexpressed LINC01518 in prostate cancer lncap cells and examined the effect of LINC01518 on gene expression profiles by RNA sequencing

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Project description:Long non-coding RNA MEG3 is widely involved in tumor development. However, its role in prostate cancer is not very clear. We overexpressed MEG3 in prostate cancer lncap cells and characterized the effect of MEG3 on gene expression profiles by RNA sequencing

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Effect of overexpression of MEG3 on gene expression in prostate cancer lncap cells

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Effect of overexpression of VIM-AS1 on gene expression in LNCaP cells

Project description:Purpose: To detect the diffirential expressed genes in LNCaP cells transfected with VIM-AS1 overexression vetor and control pcDNA3.1 vector Method: Transcriptome sequencing was sued to detect the diffirential expressed genes in LNCaP cells transfected with VIM-AS1 overexression vetor and control pcDNA3.1 vector Results :We performed transcriptome sequencing to identify the target genes in VIM-AS1 overexpressed LNCaP cells and normal control. 67 genes were found statistically up-regulated more than two-fold and 187 genes were found statistically down-regulated more than two-fold in VIM-AS1 overexpressed LNCaP cells Conclusion:Our study represents the first detailed analyasis of transcriptomes in LNCaP cells with VIM-AS1 overexpression and control cells.

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Gene expression signature overlap between shETV1 and BRD32048 in LNCaP and SK-MEL-28

Project description:Identification of BRD32048 as an inhibitor of ETV1 oncogenic transcription factor. This compound was indentified by small molecule mcroarray (a binding assay). It was able to consistently inhibit an ETV1-dependent MMP1-driven luciferase signal. Its direct binding was validated by Suface plasmon resonance (Biacore assay). It inhibits ETV1-driven invasion in ETV1-dependent cell lines. The goal of this gene expression comparison was to interogate the effects of BRD32048 on the global gene expression and to define the degree to which its siganture overlaps with an ETV1-specific shRNA-induced gene expression signature. The gene expression analysis was performed for two ETV1- dependent cell lines. (a) LNCaP (prostate cancer) uses a DOX-inducible system where two different ETV1sh (sh1117 and sh872) are induced for 4 days. In parallel cells were treated with 20 M-BM-5M BRD32048 for 16 hours. The control was DMSO treated cells. (b) SK-MEL-28 were infected with two different ETV1sh (sh3 and sh5) and selected in puromycin for 4 days. The sh control used was GFPsh. In parallel cells were treated with 20 M-BM-5M BRD32048 for 16 hours. The control was DMSO treated cells. Total RNA was isolated and measured with expression arrays. The data was normalized (see data processing) and the gene expression signatures (fold change >1.5 in either direction) were interested bteween the experimental conditions for each cell line.

2013-11-07 | E-GEOD-52154 | biostudies-arrayexpress

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