Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA227068 | ENA |
REPOSITORIES: ENA
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Project description:Dynamic interaction between prostate cancer and the bone microenvironment is a major contributor to metastasis of prostate cancer to bone. In this study we utilized an in-vitro co-culture model of PC3 prostate cancer cells and osteoblasts followed by microarray based gene expression profiling to identify previously unrecognized prostate cancer-bone microenvironment interactions. Factors secreted by PC3 cells resulted in the up-regulation of many genes in osteoblasts associated with bone metabolism and cancer metastasis, including Mmp13, Il-6 and Tgfb2, and down-regulation of Wnt inhibitor Sost. To determine whether altered Sost expression in the bone microenvironment has an effect on prostate cancer metastasis, we co-cultured PC3 cells with Sost knockout (SostKO) osteoblasts and wildtype (WT) osteoblasts and identified several genes differentially regulated between PC3-SostKO osteoblast co-cultures and PC3-WT osteoblast co-cultures. Co-culturing PC3 cells with WT osteoblasts up-regulated cancer-associated long noncoding RNA (lncRNA) MALAT1 in PC3 cells. MALAT1 expression was further enhanced when PC3 cells were co-cultured with SostKO osteoblasts and treatment with recombinant Sost down-regulated MALAT1 expression in these cells. Our results suggest that reduced Sost expression in the tumor microenvironment may promote bone metastasis by up-regulating MALAT1 in prostate cancer.
2015-09-30 | GSE73044 | GEO
Project description:We performed microarray analysis using differnt prostate cancer cell lines (PC3 and 22RV1) after TNFRSF13B (CD267) knockdown. We reported that TNFRSF13B regulates cell cycle-associated genes and P53 signaling pathway in PC3 and 22RV1 cells.
2024-02-15 | GSE196746 | GEO
Project description:Tumor-derived extracellular vesicles (EVs) play an important role in cancer pro-gression. Neutral Sphingomyelinases (nSMases) are lipid modifying enzymes that modu-late the secretion of EVs from cells. How nSMase activity and therefore ceramide genera-tion affects the composition and functionality of secreted EV is not fully understood. Here, we aimed to investigated the expression of nSMases 1 and 2 in prostate cancer (PCa) tissue and their role in EV composition and secretion for prostate cancer cell migration. Reduced nSMase 1 and 2 expression was found in prostate cancer and correlated with age of pa-tients. When nSMase 2 was inhibited by GW4869 in PCa cells, PC3 and DU145, the EV se-cretome was significantly altered, while the number of EVs and total protein content of the released EVs were not significantly changed. Using proteomics analysis, we found extra-cellular matrix proteins, such as SDC4 (Syndecan-4) and SRPX-2 differentially secreted on EVs from GW4869-treated PC3 cells. In scratch wound migration assays, GW4869 signifi-cantly increased migration compared to control PC3 cells but not DU145 cells, while SDC4 knockdown significantly reduced migration of PC3 cells. These and other nSMase 2-dependent secreted proteins are interesting candidates to understand the role of stress-induced EV in the progression of prostate cancer.
2025-05-07 | PXD062469 | Pride
Project description:We have sequenced miRNA libraries from human embryonic, neural and foetal mesenchymal stem cells. We report that the majority of miRNA genes encode mature isomers that vary in size by one or more bases at the 3’ and/or 5’ end of the miRNA. Northern blotting for individual miRNAs showed that the proportions of isomiRs expressed by a single miRNA gene often differ between cell and tissue types. IsomiRs were readily co-immunoprecipitated with Argonaute proteins in vivo and were active in luciferase assays, indicating that they are functional. Bioinformatics analysis predicts substantial differences in targeting between miRNAs with minor 5’ differences and in support of this we report that a 5’ isomiR-9-1 gained the ability to inhibit the expression of DNMT3B and NCAM2 but lost the ability to inhibit CDH1 in vitro. This result was confirmed by the use of isomiR-specific sponges. Our analysis of the miRGator database indicates that a small percentage of human miRNA genes express isomiRs as the dominant transcript in certain cell types and analysis of miRBase shows that 5’ isomiRs have replaced canonical miRNAs many times during evolution. This strongly indicates that isomiRs are of functional importance and have contributed to the evolution of miRNA genes
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Project description:PC3 are a metastatic prostate cancer cell line. Microarray analysis was performed to evaluate the impact of miR-149-3p overexpression or DAB2IP depletion in PC3.
2018-10-01 | GSE104353 | GEO
Project description:Background: The acquisition of drug resistance is one of the most malignant phenotypes of cancer. MicroRNAs (miRNAs) have been implicated in various types of cancers, but its role in taxane-resistance of prostate cancer remains poorly understood. Methods: In order to identify miRNAs related to taxane-resistance, miRNA profiling was performed using prostate cancer PC3 cells and paclitaxel-resistant PC3 cell lines established from PC3 cells. Microarray analysis of mRNA expression was also conducted to search for potential target genes of miRNA. The effects of ectopic expression of miRNA on cell growth, tubulin polymerization, drug sensitivity and apoptotic signaling pathway were investigated in a paclitaxel-resistant PC3 cell line. Results: The expression of miR-130a was down-regulated in all paclitaxel-resistant cell lines compared with parental PC3 cells. Based on mRNA microarray analysis, we identified SLAIN1 and CAV2 as potential target genes for miR-130a. Transfection with a miR-130a precursor into a paclitaxel-resistant cell line suppressed cell growth and increased the sensitivity to paclitaxel. Lastly, ectopic expression of miR-130a did not affect the polymerized tubulin level, but activated apoptotic signaling through activation of caspase-8. Conclusion: These results suggested that miR-130a may be involved in the paclitaxel-resistance and could be a therapeutic target for taxane-resistant prostate cancer.
2015-07-31 | GSE64013 | GEO