Homo sapiens
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PROVIDER: PRJNA203363 | ENA |
REPOSITORIES: ENA
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Project description:The aim of this study was to determine how gene expression is changed after arsenite-induced malignant transformation of prostate epithelial cells. Gene expression from three distinct passages of untreated, immortal RWPE-1 cells was compared to three timepoints of arsenite-exposed RWPE-1 cells (CAsE-PE) that have undergone malignant transformation.
2013-05-18 | E-GEOD-47047 | biostudies-arrayexpress
Project description:The aim of this study was to determine how gene expression is changed after arsenite-induced malignant transformation of prostate epithelial cells.
2013-05-18 | GSE47047 | GEO
Project description:Aberrant DNA methylation is frequently observed in cancer. The aim of this study was to determine how DNA methylation is changed after toxicant-induced malignant transformation. This study also puts the DNA methylation changes into context with respect to the aberrant DNA methylation events that occur in bladder and prostate carcinogenesis not associated with toxicant exposure. Immortalized UROtsa (n=3) and RWPE-1 (n=2) are compared to normal HUC (n=2) and PrEC (n=2), respectively. Arsenite (n=1), monomethylarsonous acid (n=2) or cadmium (n=1) transformed UROtsa are compared to parental UROtsa (n=3). Arsenite (n=2), cadmium (n=1) or MNU (n=1) transformed RWPE-1 cells are compared to parental RWPE-1 cells (n=2). Clinical bladder tumor biopsies (n=6), urothelial carcinoma cell lines (n=2) and prostate cancer cell lines (n=3) are compared to thier normal tissue counterparts HUC (n=2) and PrEC (n=2). Immunoprecipitation using anti-methylcytosine (5MeC) antibody.
2012-06-25 | E-GEOD-38926 | biostudies-arrayexpress
Project description:Aberrant DNA methylation is frequently observed in cancer. The aim of this study was to determine how DNA methylation is changed after toxicant-induced malignant transformation. This study also puts the DNA methylation changes into context with respect to the aberrant DNA methylation events that occur in bladder and prostate carcinogenesis not associated with toxicant exposure. Immortalized UROtsa (n=3) and RWPE-1 (n=2) are compared to normal HUC (n=2) and PrEC (n=2), respectively. Arsenite (n=1), monomethylarsonous acid (n=2) or cadmium (n=1) transformed UROtsa are compared to parental UROtsa (n=3). Arsenite (n=2), cadmium (n=1) or MNU (n=1) transformed RWPE-1 cells are compared to parental RWPE-1 cells (n=2). Clinical bladder tumor biopsies (n=6), urothelial carcinoma cell lines (n=2) and prostate cancer cell lines (n=3) are compared to thier normal tissue counterparts HUC (n=2) and PrEC (n=2). Immunoprecipitation using anti-methylcytosine (5MeC) antibody.
2012-06-25 | E-GEOD-38928 | biostudies-arrayexpress
Project description:miRNA expression profiling in malignant transformation of human bronchial epithelial cells induced by arsenite
| PRJNA392918 | ENA
Project description:miRNA Array was used to detect the expression level of miRNAs in human bronchial epithelial (HBE) cells that were transformed by a low-level arsenite exposure for 13 weeks. The transformed cells exhibited malignant phenotypes manifested by increased levels of cell proliferation, cell migration and high level of cell survival. Subsequently, 191 differentially expressed miRNAs are identified to be associated with arsenite-induced malignant transformation by employing miRNA Array. Among them, six miRNAs were chosen to validate their expression levels with qPCR and 17 miRNAs were further explored their target genes and the network. Three databases, TargetMiner, miRDB and TarBase, were used to predict the target genes of miRNAs and a total of 954 common genes were identified. Results of Gene Ontology (GO) analyses showed that these target genes were involved in diverse terms of GO categories, such as positive regulation of macroautophagy, epithelial cell maturation and synaptic vesicle clustering and so on. Moreover, results of KEGG pathway analyses demonstrated that most of these target genes were enriched in various cancer-related pathways including non-small cell lung cancer, Wnt signaling pathway, cell cycle, p53 signaling pathway and so forth. The miRNA-gene regulatory network, which was constructed by cytoscape software with miRNAs and their target genes, showed that the target genes were mainly regulated by miR-15b-5p, miR-106b-5p and miR-320d. Although more experimental verification is still needed to prove these predictions, our results may provide new insights into miRNA-mediated mechanisms underlying arsenite-induced malignant transformation.
2018-07-07 | GSE100753 | GEO
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
Project description:Background: The loss of epithelial characteristics and the acquisition of a migratory phenotype, referred to as epithelial to mesenchymal transition (EMT), is a crucial event in tumor metastasis. A better defined cell culture model for the study of EMT and its role in prostate carcinogenesis has been a challenge. Our previous work reported an EMT model based on primary prostate epithelial cells (EP156T) which gave rise to cells with mesenchymal phenotype (EPT1) without malignant transformation. Here, we present an extension of this model to stepwise malignant transformation in relation to EMT and gene expression reprogramming. Results: To achieve transformed prostate cells, EPT1 cells were kept growing in extended saturation density culture to select for cells overriding quiescence. Foci formed in EPT1 cells in 4 weeks. Cells from the foci can form robust colonies in soft agar suggesting malignant transformation. The transformed cells were named EPT2. In this stepwise transformation model, EPT2 cells showed much higher abilities to proliferation at confluence, higher resistance to apoptosis, and much lower dependence on serum and exogenous growth factors than EP156T and EPT1 cells. When EP156T and EPT1 cells at different passages were compared, only EPT1 cells at later passage but not EP156T cells could be induced to malignant transformation by high density culture. Microarray expression profiling showed that EMT and transformation were strongly connected at the gene expression level, suggesting that EMT makes EPT1 cells at later passage more susceptible to transformation induction. Conclusions: Our findings provide a novel stepwise transformation model in which EMT can emerge not only independent of transformation, but also can promote subsequent malignant transformation in prostate carcinogenesis. Dynamic changes of a core set of genes are involved in both EMT and subsequent malignant transformation.
2010-05-01 | E-TABM-949 | biostudies-arrayexpress
Project description:Transcription profiling time series of finite life span and immortal non-malignant human mammary epithelial cell lines
| PRJNA100949 | ENA
Project description: Not available
| S-EPMC2531291 | biostudies-literature