We used RNA-seq to interrogate prostate cancer specific gene fusions, alternative splicings, somatic mutations and novel transcripts. Overall design: We sequenced the transcriptome (polyA+) of 20 prostate cancer tumors and 10 matched normal tissues using Illumina GAII platform. Then we used bioinformatic approaches to identify prostate cancer specific aberrations which include gene fusion, alternative splicing, somatic mutation, etc.
Recurrent chimeric RNAs enriched in human prostate cancer identified by deep sequencing.
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View SamplesTo identify MED1 target genes involved in prostate tumorigenesis.
ERK and AKT signaling drive MED1 overexpression in prostate cancer in association with elevated proliferation and tumorigenicity.
Specimen part, Cell line
View SamplesWe have performed sucrose-gradient-based isolation of polysomal fractions from untreated and TGF-beta treated MCF-10A and MCF7 cells, subjected these fractions to RNA-seq, and also sequenced total mRNA from each cell line in the treated and untreated condition Overall design: Examination of two different cell types in a treated and untreated state
CELF1 is a central node in post-transcriptional regulatory programmes underlying EMT.
Specimen part, Treatment, Subject
View SamplesProliferation of prostate cancer cells, LNCaP, is suppressed by casodex. This suppression requires expression of AR coregulator, NCOR1.
Nuclear Receptor Corepressor 1 Expression and Output Declines with Prostate Cancer Progression.
Specimen part, Cell line
View SamplesAR transcriptional activity is regulated by DHT
Nuclear Receptor Corepressor 1 Expression and Output Declines with Prostate Cancer Progression.
Specimen part, Cell line
View SamplesCOUP-TFII, a member of the nuclear receptor superfamily plays a critical role in angiogenesis and organogenesis during embryonic development. Our results indicate that COUP-TFII expression is profoundly upregulated in prostate cancer patients and might serves as biomarker for recurrence prediction. Thus we conduct transcriptome comparison of control and COUP-TFII depleted PC3 cells to gain genomic insights on the biological processes that COUP-TFII is involved in prostate cancer cells. Ingenuity Pathway Analysis (IPA) shows that the most prominent altered pathways in the COUP-TFII depleted cells are related to cell growth; cell cycle progression and DNA damage response. Indeed many growth related genes including E2F1, p21, CDC25A, Cyclin A and Cyclin B are changed in COUP-TFII knockdown cells, suggesting that COUP-TFII might be an important regulator for prostate cancer cell growth. Further functional assays from cells and mice genetic studies confirm the hypothesis that COUP-TFII serve as the major regulator to control prostrate cancer growth. Together, results provide insight into the role of COUP-TFII in prostate tumorigenesis.
COUP-TFII inhibits TGF-β-induced growth barrier to promote prostate tumorigenesis.
Specimen part, Cell line
View SamplesWe have noticed that the proliferative potential of epithelial cells in the mouse proximal prostatic ducts is less than those at the distal prostatic ducts. To determine whether specific signaling is differentially activated in distal and proximal prostate basal cells, we isolated respective basal cells in the two regions and performed an RNA-seq analysis. Overall design: Two group comparison
Spatially Restricted Stromal Wnt Signaling Restrains Prostate Epithelial Progenitor Growth through Direct and Indirect Mechanisms.
Specimen part, Cell line, Subject
View SamplesTo identify such inhibitory signaling mediated by the stromal cells with active Wnt activity, we performed an RNA-seq analysis comparing the gene expression profiles of primarily cultured adult mouse prostate stromal cells that express S37A ß-Catenin and the control cells that only express GFP. We identified 783 genes that were differentially expressed by at least 1.2 fold (Fig. 4A). Genes associated with the Wnt receptor signaling pathway were enriched in the S37A ß-catenin group, corroborating the higher Wnt activity in this group. Overall design: Two group comparison
Spatially Restricted Stromal Wnt Signaling Restrains Prostate Epithelial Progenitor Growth through Direct and Indirect Mechanisms.
Cell line, Subject
View SamplesTo provide further insight to the signaling pathways deregulated by SPOP mutation and determine the relevance of these models to human prostate cancer, we performed RNA-seq on SPOP mutant organoids and controls. RNA-seq reads mapped to human and mouse SPOP confirmed appropriate expression of the F133V transgenic transcript without overexpression compared to endogenous mouse Spop. Quantification of gene expression was performed via RSEQtools using GENCODE as reference gene–annotation set. Both SPOPmut and SPOPwt were done in the same run. S0 was done in first run; S1 and S2 were done in second run. S3, S4 and S5 were done in third run. S5mut and S5wt were excluded from differentially expressed genes analysis, due to the different mouse line. Overall design: Differentially expressed genes between mouse SPOPmut organoids and control by RNA-seq.
SPOP Mutation Drives Prostate Tumorigenesis In Vivo through Coordinate Regulation of PI3K/mTOR and AR Signaling.
Specimen part, Subject
View SamplesBenign prostatic hyperplasia (BPH) is a common urological disease that adversely affects quality of life among elderly males, but its etiology remains poorly understood. We show that the expression of the androgen receptor (AR) is decreased in the luminal epithelial cells of human BPH specimens and is inversely correlated with the degree of regional prostatic inflammation. Overall design: To identify the extracellular signaling that promotes epithelial proliferation, we performed RNA sequencing of FACS-isolated prostate luminal cells from tamoxifen-treated control and K8-AR mice (with knockout of androgen receptor).
Non-Cell-Autonomous Regulation of Prostate Epithelial Homeostasis by Androgen Receptor.
Specimen part, Treatment, Subject
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