RNAseq analysis of prostate cancer stem cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA555090 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9699304.fastq.gz | Fastqsanger.gz | |||
| SRR9699305.fastq.gz | Fastqsanger.gz | |||
| SRR9699306.fastq.gz | Fastqsanger.gz | |||
| SRR9699307.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 4 of 4 |
Similar Datasets
Project description:Prostate cancer stem cells were isolated from PC3 cells by fluorescence activated cell sorting using the SORE6 reporter system. Differential gene expression between cancer stem cells and non-cancer stem cells were determined by RNAseq analysis.
2020-04-13 | GSE134428 | GEO
Project description:RNAseq analysis of ESRP regulated splicing events in prostate cancer
| PRJNA531685 | ENA
Project description:NKX3.1 localization to mitochondria suppresses prostate cancer initiation (Mouse 4M Prostate RNASeq)
| PRJNA474606 | ENA
Project description:There is a need to understand genetic and lifestyle factors that may influence the risk of cancer progression in men who have organ-confined prostate cancer and have chosen a programme of 'active surveillance' as opposed to radical treatment with the associated health risks. Epidemiological studies have suggested that consumption of cruciferous vegetables is associated with reduced risk of developing aggressive prostate cancer. In this study we recruited men on active surveillance for low- to intermediate-risk prostate cancer to determine whether a 12-month dietary intervention can elicit transcriptional or nmetabolic responses in their prostate that would be consistent with a reduction in the risk of progression. We undertook RNAseq on prostate biopsies collected before and after a 12-month intervention with broccoli soups.
2020-01-01 | E-MTAB-6525 | biostudies-arrayexpress
Project description:Aggressive cancers and normal stem cells often share similar molecular and functional traits. It is unclear if aggressive phenotypes of prostate cancer molecularly resemble normal stem cells residing within the human prostate. We performed high-throughput RNA sequencing on uncultured, highly purified epithelial populations from human prostates obtained after radical prostatectomy. We found the basal population to be defined by genes associated with developmental programs, epigenetic remodeling, and invasiveness. We further generated a 91-gene basal signature and applied it to gene expression datasets from patients with organ-confined or castration-resistant, metastatic prostate cancer. Metastatic prostate cancer was more enriched for the basal stem cell signature than organ-confined prostate cancer. Moreover, histological subtypes within prostate cancer metastases varied in their enrichment of the stem cell signature with small cell neuroendocrine carcinoma being the most stem cell-like. Bioinformatic analysis of the basal cell and two human small cell gene signatures identified a set of E2F target genes common to all three signatures. These results suggest that the most aggressive variants of prostate cancer share a core transcriptional program with normal prostate basal stem cells. Transcriptional analysis of 10 uncultured prostatic basal and luminal populations from either the benign or malignant prostate tissue of 8 human prostate cancer patients by high-throughput RNA-seq
2016-06-01 | E-GEOD-82071 | biostudies-arrayexpress
Project description:Gene expression of sphere-derived prostate cancer stem cells
| PRJNA948672 | ENA
Project description:Progression of prostate cancer -the most frequent cancer in men- is driven by androgen steroid hormones, and delayed by androgen deprivation therapy (ADT). Androgens control transcription in prostate cancer cells by stimulating androgen receptor (AR) activity, but also control pre-mRNA splicing through less clear mechanisms. Here we examine whether androgens regulate splicing through AR-mediated transcriptional control of splicing regulator proteins. Supporting this mechanism we find AR controls ESRP2, which encodes a key epithelial-specific splicing regulator. Both ESRP2 and its close paralog ESRP1 are highly expressed in primary prostate cancer, and slow growth of prostate cancer xenografts in mice. Androgen stimulation induces splicing switches in many endogenous ESRP2-controlled mRNA isoforms, including a key splicing switch in the metastatic regulator FLNB which is associated with disease relapse after treatment. ESRP2 expression in clinical prostate cancer is repressed by ADT, which may thus inadvertently dampen epithelial splice programmes. Supporting this, FLNB splicing was reciprocally switched by the AR antagonist Casodex®. Our data reveal a new mechanism of splicing control in prostate cancer with important implications for disease progression.
2019-09-06 | GSE129540 | GEO
Project description:Aggressive cancers and normal stem cells often share similar molecular and functional traits. It is unclear if aggressive phenotypes of prostate cancer molecularly resemble normal stem cells residing within the human prostate. We performed high-throughput RNA sequencing on uncultured, highly purified epithelial populations from human prostates obtained after radical prostatectomy. We found the basal population to be defined by genes associated with developmental programs, epigenetic remodeling, and invasiveness. We further generated a 91-gene basal signature and applied it to gene expression datasets from patients with organ-confined or castration-resistant, metastatic prostate cancer. Metastatic prostate cancer was more enriched for the basal stem cell signature than organ-confined prostate cancer. Moreover, histological subtypes within prostate cancer metastases varied in their enrichment of the stem cell signature with small cell neuroendocrine carcinoma being the most stem cell-like. Bioinformatic analysis of the basal cell and two human small cell gene signatures identified a set of E2F target genes common to all three signatures. These results suggest that the most aggressive variants of prostate cancer share a core transcriptional program with normal prostate basal stem cells.
2016-06-01 | GSE82071 | GEO
Project description:Purpose: The goal of this study is to identify transcriptome-wide changes that occur in a mouse prostate cell line with knockdown of Map3k7(Tak1) and Chd1. We utilize this cell line as a model of an aggressive prostate cancer subtype consisting of loss of both MAP3K7 and CHD1 in human patients. RNAseq comparing shControl, shMap3k7(Tak1), shChd1, and shDouble (both) was used to identify transcriptome changes resulting from loss of these genes of interest in order to identify potential therapeutic vulnerabilites. Cell line: The generation of the WFU3 cell line has been previously described (Barclay, W.W et al. The Prostate. 2005; PMID:15599944). Breifly, anterior prostate lobes of adult B1/6; 129/SVEV mice were harvested, minced, and extensively digested, and resulting organoids were separated from stromal cells using a Percoll density gradient. These organoids were then plated on rat-tail collagen coated plates in complete growth media, and after 4-5 passages were transferred to uncoated plates. These prostatic epithelial progenitor stem cells are maintained in supplemented 50:50 Dulbecco’s modified Eagle’s medium (DMEM)/Ham’s F-12 medium (F12). Complete media components are described in the Barclay, W.W paper.
2019-07-01 | GSE132664 | GEO