Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA134387 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR071160.fastq.gz | Fastqsanger.gz | |||
| SRR071161.fastq.gz | Fastqsanger.gz | |||
| SRR071162.fastq.gz | Fastqsanger.gz |
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Project description:The stromal microenvironment plays key roles in prostate development and cancer. Cancer associated fibroblasts (CAFs) and other stromal cells stimulate tumourigenesis via several mechanisms including the expression of pro-tumourigenic factors. Mesenchyme (embryonic stroma) controls prostate organogenesis, and in some circumstances can re-differentiate prostate tumours. Epithelia are regulated by powerful paracrine signalling from the stroma in both development and disease, and identification of these stromal signals is important. We have applied next-generation Tag profiling to fetal human prostate, normal human prostate fibroblasts (NPFs) and CAFs to identify molecules expressed in prostatic stroma Each sample was used for Tag library construction, by Solexa Inc
2011-10-22 | E-GEOD-25018 | biostudies-arrayexpress
Project description:The stromal microenvironment plays key roles in prostate development and cancer. Cancer associated fibroblasts (CAFs) and other stromal cells stimulate tumourigenesis via several mechanisms including the expression of pro-tumourigenic factors. Mesenchyme (embryonic stroma) controls prostate organogenesis, and in some circumstances can re-differentiate prostate tumours. Epithelia are regulated by powerful paracrine signalling from the stroma in both development and disease, and identification of these stromal signals is important. We have applied next-generation Tag profiling to fetal human prostate, normal human prostate fibroblasts (NPFs) and CAFs to identify molecules expressed in prostatic stroma
2011-10-22 | GSE25018 | GEO
Project description:We applied ChIPseq to identify genomic AR binding sites for the first time in primary human fetal prostate fibroblasts and patient derived cancer associated fibroblasts, as well as the WPMY1 cell line overexpressing AR. We identified AR binding sites that were specific to fetal prostate fibroblasts (7534), cancer fibroblasts (629), WPMY1-AR (2561) as well as those common among all (783). Primary fibroblasts had a distinct AR binding profile versus prostate cancer cell lines and tissue, and showed a localisation to gene promoter binding sites 1kb upstream of the transcriptional start site, as well as non-classical AR binding sequence motifs. We used RNAseq to define transcribed genes associated with AR binding sites and derived cistromes for embryonic and cancer fibroblasts as well as a cistrome common to both. These were compared to several in vivo ChIPseq and transcript expression datasets; which identified subsets of AR targets that were expressed in vivo and regulated by androgens in order to define for the first time which cellular subpopulations might be the true source of AR-associated signals.
2017-05-24 | GSE90772 | GEO
Project description:Background The characteristics of a tumor are largely determined by its interaction with the surrounding micro-environment (TME). TME consists of both cellular and non-cellular components. Cancer-associated fibroblasts (CAFs) are a major component of the TME. They are a source of many secreted factors that influence the survival and progression of tumors as well as their response to drugs. Identification of markers either overexpressed in CAFs or unique to CAFs would pave the way for novel therapeutic strategies that in combination with conventional chemotherapy are likely to have better patient outcome. Methods Fibroblasts have been derived from Benign Prostatic Hyperplasia (BPH) and prostate cancer. RNA from these has been used to perform a transcriptome analysis in order to get a comparative profile of normal and cancer-associated fibroblasts. Results The study has identified 818 differentially expressed mRNAs and 17 lincRNAs between normal and cancer-associated fibroblasts. Also, 15 potential lincRNA-miRNA-mRNA combinations have been identified which may be potential biomarkers. Conclusions Identified differentially expressed markers between normal and cancer-associated fibroblasts would help in CAFs/derived factors targeted therapy in combination with conventional therapy. However, this would in future need more experimental validation.
2024-09-26 | GSE270705 | GEO
Project description:A greater understanding of cell signaling events that occur within the prostate cancer tumor microenvironment (TME), for example between cancer-associated fibroblasts (CAFs) and prostate epithelial or cancer cells, may identify novel biomarkers and more effective therapeutic strategies for this disease. To address this, we used cell-type specific labelling with amino acid precursors (CTAP) to define cell type-specific phosphoproteomic changes that occur when prostate epithelial cells are co-cultured with normal patient-derived prostate fibroblasts (NPFs) versus matched CAFs.
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Project description:Currently, comprehensive and quantitative proteomic analysis of human prostate cancer tissue specimens remains scarce, hindering the identification of protein complexes and pathways deregulated in prostate cancer. In this study, we applied TMT-SPS-MS3-based quantitative proteomics to analzye 9 normal controls, 9 low-grade prostate cancer, and 9 high-grade prostate cancer. About 3,600 proteins were quantified across all the 27 prostate specimens. Statistical analysis identified 651 proteins that are differentially expressed in high-grade prostate cancer and normal prostate. Pathway enrichment analysis revealed that the LXR/RXR activation and integrin signaling pathways are substantially downregulated in high-grade prostate cancer, compared with normal prostate cancer. In addition, protein complex analysis suggested that mitochondrial ribosomes and ribosome-biogenesis complexes are significnatly overexpressed, whereas the cholesterol effluex and focal adhesion comlexes are significantly downregulated in high-grade prostate cancer, compared with normal controls. Furthermore, differential correlation analysis indicated that the spliceosome machinery might be more active in low-grade prostate cancer, compared with normal controls. The results are expected to shed light on the molecular mechnanisms underlying the development and progression of primary prostate cancer in human patients.
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Project description:Prostate cancer is a biologically heterogeneous disease with considerable variation in clinical aggressiveness. The behavior of prostate cancer can be considered a direct or indirect result of aberrant alterations of gene expression in prostate epithelial cells. Identification of the patterns of gene-expression alterations that are related to the aggressiveness of prostate cancers will greatly assist the development of tools for early detection of prostate cancers with poor clinical outcome and identification of targets for future therapeutic intervention. To detect the patterns of gene-expression alterations of prostate cancers, we performed a comprehensive gene-expression analysis on 30 prostate tissues of various levels of invasiveness (ranging from those confined to the organ to distant metastases) and Gleason grades (combined scores 4-9), using the Affymetrix chip set Hu35k (A-D) and U95a. Following three sequential selection screens, we identified 84 largely novel genes and expressed sequence tag (EST) sequences whose expression levels were altered significantly in prostate cancer samples compared with control normal tissues. In addition, the expression levels of a group of 12 genes and EST sequences was found to be altered significantly in aggressive type of prostate cancers but not in organ-confined prostate cancers. Cluster analysis using the 84-gene list showed that the highly aggressive prostate cancers contained gene-expression patterns that were distinct from organ-confined prostate cancers ( Molecular Carcinogenesis 33:25-35, 2002). becic-00229 Assay Type: Gene Expression Provider: Affymetrix Array Designs: Hu35KsubA Organism: Homo sapiens (ncbitax) Tissue Sites: Prostate Material Types: synthetic_DNA, synthetic_RNA, organism_part Disease States: Normal, Prostate_Adenocarcinoma
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Project description:Prostate cancer is a biologically heterogeneous disease with considerable variation in clinical aggressiveness. The behavior of prostate cancer can be considered a direct or indirect result of aberrant alterations of gene expression in prostate epithelial cells. Identification of the patterns of gene-expression alterations that are related to the aggressiveness of prostate cancers will greatly assist the development of tools for early detection of prostate cancers with poor clinical outcome and identification of targets for future therapeutic intervention. To detect the patterns of gene-expression alterations of prostate cancers, we performed a comprehensive gene-expression analysis on 30 prostate tissues of various levels of invasiveness (ranging from those confined to the organ to distant metastases) and Gleason grades (combined scores 4-9), using the Affymetrix chip set Hu35k (A-D) and U95a. Following three sequential selection screens, we identified 84 largely novel genes and expressed sequence tag (EST) sequences whose expression levels were altered significantly in prostate cancer samples compared with control normal tissues. In addition, the expression levels of a group of 12 genes and EST sequences was found to be altered significantly in aggressive type of prostate cancers but not in organ-confined prostate cancers. Cluster analysis using the 84-gene list showed that the highly aggressive prostate cancers contained gene-expression patterns that were distinct from organ-confined prostate cancers ( Molecular Carcinogenesis 33:25-35, 2002).
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Project description:Comparison of Normal Prostate Fibroblasts Overexpressing Cyclin D1 and Carcinoma Associated Fibroblasts
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