Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA188955 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Sodium arsenite induced gene expression changes in A549 human epithelial lung carcinoma cells
| PRJNA188954 | ENA
Project description:Arsenic is methylated during its metabolism, thereby depleting the intracellular methyl donor S-adenosyl-methionine, which may lead to disturbances in DNA methylation patterns Cells were exposed to sodium arsenite (NaAsO2, Sigma) at concentrations of 0.08 M-BM-5M, 0.4 M-BM-5M and 2 M-BM-5M for 1, 2 and 8 weeks. A549 arsenic dose time response study.
2014-09-17 | E-GEOD-44173 | biostudies-arrayexpress
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 Most of these temporal patterns in gene expression are reversed when arsenic was withdrawn.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
Project description:Sodium arsenite effects on DNA methylation in zebrafish embryos.
| PRJNA355643 | ENA
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:Genome-wide DNA-methylation profiles of human lung cancer cell lines and normal lung cells were generated by Infinium bead chip technology DNA methylation patterns of over 480,000 CpG sites were analyzed in normal human bronchial epithelial cells (NHBEC) and three non small cell lung cancer cell lines (NSCLC: A427, A549 and H322) using bisulfite-based Illumina 450K BeadChip arrays
2017-08-15 | GSE92843 | GEO
Project description:This study was carried out to compare the changes in gene expression in 5 dpf zebrafish larval livers in response to mutation of the arsenic methylation gene (as3mt) - 8 bp deletion in exon 3 with and without 1 mM sodium arsenite treatment (96-120 hpf)
2023-05-01 | GSE228752 | GEO
Project description:There is a need to develop biomarkers in alternative testing models predictive for chemically induced chronic disease in humans, preferably describing key events and their relationships in an adverse outcome pathway analysis. Epigenetic modifications, and particularly DNA methylation effects, have been implicated as a major event in susceptibility to develop chronic disease. Arsenic exposure affects large populations around the world through drinking water and industrial activities. We sought to identify epigenetic markers of arsenic exposure. We analyzed the effect of sodium arsenite on DNA methylation in Danio rerio (zebrafish) embryos using unbiased methylation profiling by high throughput sequencing.
2017-10-19 | GSE90735 | GEO