Project description:MiRNAs are small non-coding RNAs that regulate the expression of specific mRNA targets mainly by translational repression, mRNA deadenylation or cleavage. This series is meant to identify miRNAs deregulated in prostate cancer (PCa) by comparing the PCa cell lines LNCaP, PC3 and Du-145 to the normal prostate epithelial cell line RWPE-1. We analyzed three arrays each for LNCaP, PC3, Du-145 and RWPE-1 cell lines
Project description:This SuperSeries is composed of the following subset Series: GSE17315: mRNA expression upon reconstitution of miR-130a, miR-203 and miR-205 in prostate cancer cell line LNCaP GSE17317: miRNA expression in LNCaP, PC3, Du-145 and RWPE-1 cell lines GSE22979: Profiling of direct mRNA targets of miR-130a, miR-203 and miR-205 in prostate cancer cell line LNCaP Refer to individual Series
Project description:MiRNAs are small non-coding RNAs that regulate the expression of specific mRNA targets mainly by translational repression, mRNA deadenylation or cleavage. This series is meant to identify miRNAs deregulated in prostate cancer (PCa) by comparing the PCa cell lines LNCaP, PC3 and Du-145 to the normal prostate epithelial cell line RWPE-1.
Project description:DNA-methylation targets specific for urothelial cancer (UC) were identified by genome-wide methylation difference analysis of human urothelial (RT4, J82, 5637), prostate (LNCAP, DU-145, PC3) and renal (RCC-KP, CAKI-2, CAL-54) cancer cell lines with their respective primary epithelial cells
Project description:Prostate cancer (PCa) is the most common malignant carcinoma that develops in men in Western countries. Up to 30% of patients continue to suffer from disease progression following radical prostatectomy. Therefore, better prognostic markers and molecular targets for cancer treatment are needed. MicroRNA (miRNA) has the potential to be used as biomarkers and as a therapeutic target for the treatment of various cancers, including PCa. Here, to determine how miRNA is involved in PCa progression, we investigated the miRNA expression profiles of 3 PCa cell lines, namely PC3, DU145, and LNCaP, and 2 normal prostate cell lines, namely RWPE-1 and PrSc, using miRNA microarrays. We investigated miRNA genes that were significantly upregulated in PCa cell lines (PC3, DU145, LNCaP) compared with normal cell lines (RWPE-1, PrSc).
Project description:We conducted gene expression profilling of common prostate cell lines for comparison with genome-wide DNA methylation profiles for the same cell lines to study the impact of differential DNA methylation in prostate cancer. Total RNA was extracted from 3 biological replicate sets of PrEC, RWPE-1, DU 145, and LNCaP cells. This Series represents the gene expression profiling data only. The methyl-Seq data were submitted directly to SRA and are represented by accession SRA049689.1.
Project description:Disseminated prostate cancer cells colonize the skeleton to progress into macroscopic lesions only if they successfully adapt to the bone microenvironment. We previously reported that the ability of prostate cancer cells to generate skeletal tumors in animal models correlated with the expression of the alpha-receptor for Platelet-Derived Growth Factor (PDGFRa). In this study we aimed to identify PDGFRa-regulated genes responsible for the acquisition of a bone-metastatic prostate phenotype. We performed genome-wide expression comparative analyses of human prostate cancer cell lines that differ for PDGFRa expression and propensity to establish tumors in the skeleton of animal models. We investigated the genes that were differentially regulated in the highly bone-metastatic PC3-ML cells and their low-metastatic counterpart PC3-N cells, and the genes differentially regulated between PC3-N and PC3-N with overexpression of PDGFRa (PC3NRa). We have previously shown that DU-145 cells lack PDGFRa and fail to survive longer than three days as disseminated tumor cells after homing to the mouse bone marrow. Interestingly, and in contrast to PC3-N cells, the exogenous expression of PDGFRa did not promote metastatic bone-tropism of DU-145 cells in our model. Thus, we examined the genes that were differentially regulated between DU-145 and DU-145(Ra) and excluded them from our candidate genes. Finally, to refine our findings and compensate for PC3 and DU-145 genetic disparity, we performed a comparative analysis of the genes differentially regulated between two bone metastatic single-cell progenies that were derived from PC3-ML cells.
Project description:Gene expression of 5 prostate cancer cell lines (LNCaP, VCaP, DU-145, PC-3, DuCaP) in standard culture conditions, harvested during exponential growth phase.
Project description:Disseminated prostate cancer cells colonize the skeleton to progress into macroscopic lesions only if they successfully adapt to the bone microenvironment. We previously reported that the ability of prostate cancer cells to generate skeletal tumors in animal models correlated with the expression of the alpha-receptor for Platelet-Derived Growth Factor (PDGFRa). In this study we aimed to identify PDGFRa-regulated genes responsible for the acquisition of a bone-metastatic prostate phenotype. We performed genome-wide expression comparative analyses of human prostate cancer cell lines that differ for PDGFRa expression and propensity to establish tumors in the skeleton of animal models. We investigated the genes that were differentially regulated in the highly bone-metastatic PC3-ML cells and their low-metastatic counterpart PC3-N cells, and the genes differentially regulated between PC3-N and PC3-N with overexpression of PDGFRa (PC3NRa). We have previously shown that DU-145 cells lack PDGFRa and fail to survive longer than three days as disseminated tumor cells after homing to the mouse bone marrow. Interestingly, and in contrast to PC3-N cells, the exogenous expression of PDGFRa did not promote metastatic bone-tropism of DU-145 cells in our model. Thus, we examined the genes that were differentially regulated between DU-145 and DU-145(Ra) and excluded them from our candidate genes. Finally, to refine our findings and compensate for PC3 and DU-145 genetic disparity, we performed a comparative analysis of the genes differentially regulated between two bone metastatic single-cell progenies that were derived from PC3-ML cells. Seven human prostate cancer cell lines were analyzed in total for this study. Each cell line was analyzed in duplicate from two different passages in culture.