Gene expression data from immortal and arsenite-transformed malignant prostate epithelial cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE47047 | GEO | 2013/05/18
SECONDARY ACCESSION(S): PRJNA203363
REPOSITORIES: GEO
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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: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 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:Aberrant DNA methylation is frequently observed in cancer. The aim of this study was to determine how DNA methylation is changed after arsenic-induced malignant transformation. Arsenite-transformed RWPE-1 cells (n=2) are compared to parental RWPE-1 cells (n=2). Normal PrEC (n=2) are included for comparison. Immunoprecipitation using anti-methylcytosine (5MeC) antibody.
2012-06-25 | E-GEOD-38929 | biostudies-arrayexpress
Project description:Proteome characterization of gland confined prostate tumors and non-malignant prostate tissue. Whole cell protein extracts were purified from FFPE radical prostatectomy specimens for a total of 28 tumor samples and 8 adjacent non-malignant prostate tissues. Associated ProteomeXchange identifiers: PXD003430, PXD003452, PXD003515, PXD004132, PXD003615, PXD003636. Quantitative proteomic analysis of adjacent non-malignant prostate tissue (n=8) and gland confined prostate tumors (n=28) obtained from radical prostatectomy procedures; and bone metastatic prostate tumors (n=22) obtained from patients operated to relief spinal cord compression. At the time of surgery, most metastatic patients had relapsed after androgen-deprivation therapy, while 5 were previously untreated.
2018-08-21 | PXD009868 | Pride
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.
2012-06-26 | GSE38928 | 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.
2012-06-26 | GSE38926 | 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 arsenic-induced malignant transformation.
2012-06-26 | GSE38929 | GEO
Project description:Arsenic (As) exposure is a significant worldwide environmental health concern. Low dose, chronic arsenic exposure has been associated with higher risk of skin, lung, and bladder cancer, as well as cardiovascular disease and diabetes. While arsenic-induced biological changes play a role in disease pathology, little is known about the dynamic cellular changes due to arsenic exposure and withdrawal. In these studies, we seek to understand the molecular mechanisms behind the biological changes induced by chronic low doses of arsenic exposure. We used a comprehensive approach involving chromatin structural studies and mRNA microarray analyses to determine how chromatin structure and gene expression patterns change in response to chronic low dose arsenic exposure and its subsequent withdrawal. Our results show that cells exposed to low doses of sodium arsenite have distinct temporal and coordinated chromatin, gene expression and miRNA changes that are consistent with differentiation and activation of multiple biochemical pathways. Most of these temporal patterns in gene expression are reversed when arsenic was withdrawn. However, some of the gene expression patterns remained altered, plausibly as a result of an adaptive response by these cells. Additionally, these gene expression patterns correlated with changes in chromatin structure, further solidifying the role of chromatin structure in gene regulatory changes due to arsenite exposure. Lastly, we show that arsenite exposure influences gene regulation both at the transcription initiation as well as at the splicing level. Thus our results suggest that general patterns of alternative splicing, as well as expression of particular gene regulators, can be indicative of arsenite-induced cell transformation. A total of eight (8) samples with two biological replicates under four separate conditions: wild-type treated with deionized H2O for 36 days (NT); chronic low-dose arsenic exposure of 1 uM of sodium arsenite (iAs-T) for 36 days; chronic arsenic exposure of 1 uM of sodium arsenite for 26 days followed by removal of sodium arsenite for 10 days, measured at day 36 (iAs-Rev); and chronic arsenic exposure of 1 uM of sodium arsenite for 26 days, followed by removal of sodium arsenite exposure for 10 days, followed by 1 uM of chronic sodium arsenite exposure for 10 days (measured at day 46) (iAs-Rev-T).
2015-05-05 | E-GEOD-60760 | biostudies-arrayexpress