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Homo sapiens

ABSTRACT: GATA2 shRNA Expression in Castration Resistant Prostate Cancer Cell Lines

PROVIDER: PRJNA254050 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1503200.fastq.gz	Fastqsanger.gz
	SRR1503210.fastq.gz	Fastqsanger.gz
	SRR1503220.fastq.gz	Fastqsanger.gz
	SRR1503201.fastq.gz	Fastqsanger.gz
	SRR1503211.fastq.gz	Fastqsanger.gz

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GATA2 shRNA Expression in Castration Resistant Prostate Cancer Cell Lines

Project description:The transcription factor GATA2 regulates chemotherapy resistance in prostate cancer. We report a novel GATA2 transcriptional program that has implications for chemotherapy resistance disease and aggressiveness in castration resistant prostate cancer. Examination of the transcriptional network changes induced in human Ch-CRPC cell lines by two shRNA mediated knock down of GATA2 versus random shRNA control

2014-11-04 | E-GEOD-58966 | biostudies-arrayexpress

GATA2 shRNA Expression in Castration Resistant Prostate Cancer Cell Lines

2014-11-04 | GSE58966 | GEO

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Project description:Castration-Resistant Prostate Cancer (CRPC)

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Epigenetic Activation and alteration of chromatin structure regulated by NSD2 in metastatic castration-resistant prostate cancer (Hi-C)

Project description:To elucidate the regulation of NSD2 in metastatic castration-resistant prostate cancer(CRPC), we performed Hi-C against castration-sensitive prostate cancer cell line LNCaP and metastatic castration-resistant prostate cancer cell lines, PC3 respectively. In metastatic CRPC, we found specific regions of activation with epigenetic changes.

2024-09-04 | GSE248627 | GEO

Epigenetic Activation and alteration of chromatin structure regulated by NSD2 in metastatic castration-resistant prostate cancer (ChIP-seq)

Project description:To elucidate the regulation of NSD2 in metastatic castration-resistant prostate cancer(CRPC), we performed ChIP-seq of H3K36me2, H3K27me3, H3K4me1, H3K4me3,H3K27ac and NSD2 against castration-sensitive prostate cancer cell line LNCaP and metastatic castration-resistant prostate cancer cell lines, PC3 and DU145, respectively. In metastatic CRPC, we found specific regions of activation with epigenetic changes.

2024-09-04 | GSE248629 | GEO

Epigenetic Activation and alteration of chromatin structure regulated by NSD2 in metastatic castration-resistant prostate cancer (RNA-seq)

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Gene Expression in Castration-Resistant C4-2 Cells after AR Knockdown

Project description:Prostate cancer is the most common, lethal malignancy in men. Although androgen withdrawal therapies are used to treat advanced disease, progression to a castration-resistant, end-stage is the usual outcome. In this study, the tested hypothesis was that the androgen receptor remains essential for the growth and viability of castration-resistant disease. Knocking down the androgen receptor in well-established tumors grown in castrated mice caused growth arrest, decreased serum PSA, and frequently regression and total eradication of tumors. Growth control of castration-resistant tumors appeared to be linked to the extent of androgen receptor knockdown, which triggers upregulation of many genes involved in apoptosis, cell cycle arrest, and inhibition of tumorigenesis and protein synthesis. Our findings provide proof of principle that in vivo knockdown of the androgen receptor is a viable therapeutic strategy to control and possibly eradicate prostate cancers that have progressed to the lethal castration-resistant state. C4-2 human prostate cancer cells stably expressing a tetracycline-inducible AR-targeted short hairpin RNA (shRNA) or scrambled shRNA were generated. These two cell lines were incubated in the absence of androgens with or without doxycycline hyclase (DOX). Comparison analysis of the gene expression profiles of C4-2 cells stably expressing AR shRNA + DOX and control cells (AR shRNA - DOX and scrambled shRNA Â± DOX) was conducted to identify differentially regulated genes due to AR knockdown after normalization and data filtering. Genes were considered to be significantly different if the expression in the induced AR shRNA + DOX cells was at least 1.7-fold greater or 1.7-fold less than that seen in the control cells, with P< 0.05.

2010-06-23 | E-GEOD-13332 | biostudies-arrayexpress

Homo sapiens

Project description:Altered expression of long noncoding RNAs in LNCaP castration resistant prostate cancer cell lines

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Project description:Androgen receptor splice variants mediate enzalutamide resistance in castration-resistant prostate cancer cell lines

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RNA-seq of human prostate cancer cell lines grown as orthotopic tumour models of castration resistant prostate cancer

Project description:To identify changes at multiple omic levels between hormone naive and castration resistant prostate cancer. Using orthograft murine tumour models of human cell lines injected into the prostate of CD-1 Nude mice grown under castration resistant (castrate) or hormone naive (non-castrate) conditions.

2021-05-03 | E-MTAB-9831 | biostudies-arrayexpress

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