Homo sapiens
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PROVIDER: PRJNA101767 | ENA |
REPOSITORIES: ENA
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Project description:The alkylating agent N-methyl-N’-nitro-N-nitrosoguanidine (MNNG) induces cellular DNA damages and other comprehensive alterations that lead to chromosomal aberrations, mutations, tumor initiations, and cell death. However, the molecular mechanism of MNNG-induced cellular stress remains unclear.We have genome-wide analyzed early transcriptional responses of human FL amnion epithelial cells after exposure to three relatively low doses of MNNG (0.2, 1.0, and 10.0µM),and differential gene expression profiles were obtained 4 h after exposure using oligonucleotide microarrays followed by validation with quantitative real-time RT-PCR. The results demonstrate that the MNNG-responsive genes are involved in multiple cellular biological processes including transcription regulation, signal transduction, cell cycle regulation, cytoskeleton organization, protein synthesis, immune response, metabolism, etc. The possible roles of these genes and their related pathways in MNNG-induced cellular responses were discussed. This study helps to draw the whole picture how cells respond to environmental chemical exposure via transcriptional regulation. Experiment Overall Design: Human amnion epithelial FL cells were exposed to vehicle control (dimethyl sulfoxide) and increasing doses(0.2, 1.0, and 10.0µM)of N-methyl-N’-nitro-N-nitrosoguanidine(MNNG), respectively. The transcriptomes of the three treatments were compared to that of the control, respectively, to test the hypothesis that a characterized differential expression profile would be generated by exposure to various doses of this genotoxic agent.
2009-01-09 | E-GEOD-8602 | biostudies-arrayexpress
Project description:The alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) is a direct mutagen and carcinogen, causing DNA damage and other comprehensive alterations that lead to chromosomal aberrations, mutations, tumor initiation, and cell death. Our previous study revealed that MNNG at different concentrations could induce extensive changes in gene expression at an early stage of exposure. To further understand the dynamic cellular responses and hazardous effects caused by this environmental carcinogen, we used a whole-genome time-course screening methods to find out the gene expression changes induced by a low concentration of MNNG in human normal amnion epithelial FL cells. The cells were exposed to 1.0 M-BM-5M MNNG, and differential gene expression profiles at 3, 12, and 24 h after MNNG treatment were obtained by use of Affymetrix HG-U133 Plus 2.0 oligonucleotide microarray technology, followed by quantitative real-time RT-PCR validation. The results showed that the low-dose MNNG exposure triggered extensive but moderate changes in gene expression at these three experiment time points after exposure. The responsive genes encode important proteins, including cell cycle regulators, transcription factors and signal transducers that determine cell cycle progression, cell fate and other activities associate with pro-oncogenic potentials. The differential gene expression profiles at the three time points varied greatly, and generally reflected a cellular responsive process from initiation to progression and to recovery after MNNG exposure. These results will aid our understanding of the complicated mechanisms of MNNG-induced cellular responses. KeywordsM-oM-<M-^ZN-methyl-N'-nitro-N-nitrosoguanidine; Cellular response; Temporal gene expression change; Oligonucleotide microarray; Quantitative real-time RT-PCR Human amnion epithelial FL cells were exposed to vehicle control (dimethyl sulfoxide) and a low concentration (1.0 M-BM-5M) MNNG for 2 h, respectively. The differential gene expression profiles at 3, 12 and 24 h post MNNG treatment were obtained using Affymetrix HG-U133 Plus 2.0 oligonucleotide microarrays. The transcriptomic changes at different time points post MNNG treatment would provide insight into the dynamic processes of cellular response to this genotoxic agent.
2013-07-01 | E-GEOD-21270 | biostudies-arrayexpress
Project description:The alkylating agent N-methyl-N’-nitro-N-nitrosoguanidine (MNNG) induces cellular DNA damages and other comprehensive alterations that lead to chromosomal aberrations, mutations, tumor initiations, and cell death. However, the molecular mechanism of MNNG-induced cellular stress remains unclear.We have genome-wide analyzed early transcriptional responses of human FL amnion epithelial cells after exposure to three relatively low doses of MNNG (0.2, 1.0, and 10.0µM),and differential gene expression profiles were obtained 4 h after exposure using oligonucleotide microarrays followed by validation with quantitative real-time RT-PCR. The results demonstrate that the MNNG-responsive genes are involved in multiple cellular biological processes including transcription regulation, signal transduction, cell cycle regulation, cytoskeleton organization, protein synthesis, immune response, metabolism, etc. The possible roles of these genes and their related pathways in MNNG-induced cellular responses were discussed. This study helps to draw the whole picture how cells respond to environmental chemical exposure via transcriptional regulation. Keywords: Dose response
2009-01-01 | GSE8602 | GEO
Project description:The alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) is a direct mutagen and carcinogen, causing DNA damage and other comprehensive alterations that lead to chromosomal aberrations, mutations, tumor initiation, and cell death. Our previous study revealed that MNNG at different concentrations could induce extensive changes in gene expression at an early stage of exposure. To further understand the dynamic cellular responses and hazardous effects caused by this environmental carcinogen, we used a whole-genome time-course screening methods to find out the gene expression changes induced by a low concentration of MNNG in human normal amnion epithelial FL cells. The cells were exposed to 1.0 µM MNNG, and differential gene expression profiles at 3, 12, and 24 h after MNNG treatment were obtained by use of Affymetrix HG-U133 Plus 2.0 oligonucleotide microarray technology, followed by quantitative real-time RT-PCR validation. The results showed that the low-dose MNNG exposure triggered extensive but moderate changes in gene expression at these three experiment time points after exposure. The responsive genes encode important proteins, including cell cycle regulators, transcription factors and signal transducers that determine cell cycle progression, cell fate and other activities associate with pro-oncogenic potentials. The differential gene expression profiles at the three time points varied greatly, and generally reflected a cellular responsive process from initiation to progression and to recovery after MNNG exposure. These results will aid our understanding of the complicated mechanisms of MNNG-induced cellular responses. Keywords：N-methyl-N'-nitro-N-nitrosoguanidine; Cellular response; Temporal gene expression change; Oligonucleotide microarray; Quantitative real-time RT-PCR
2013-07-01 | GSE21270 | GEO
Project description:Genotoxic agents cause cellular DNA damage and stress responses, including transcriptional changes. Here we focused on the early transcriptional responses of human cells to benzo(a)pyrene diol epoxide (BPDE), which causes bulky DNA adduct damage. Human amnion epithelial FL cells were exposed to three doses of BPDE (5, 50, and 500 nM) and the vehicle control DMSO, and differential gene expression profiles were obtained 4 h after exposure using oligonucleotide microarrays followed by validation with quantitative real-time RT-PCR. Compared with a few genes affected by the low and medium-dose exposure, extensive and robust changes in gene expression were induced by the high-dose BPDE. We found that the expression of cell cycle-regulators, signaling molecules and transcription factors were significantly altered and important signaling pathways related to cell survival or apoptosis were affected by BPDE. Several genes and related regulatory pathways that were previously not known to be responsive to this genotoxic agent have now been implicated, which helps to draw the whole picture of how cells respond to environmental chemical exposure via transcriptional regulation. Experiment Overall Design: Human amnion epithelial FL cells were exposed to vehicle control (dimethyl sulfoxide) and increasing doses (5, 50, 500 nM) of anti-benzo(a)pyrene diol epoxide (anti-BPDE), respectively. The transcriptomes of the three treatments were compared to that of the control, respectively, to test the hypothesis that a characterized differential expression profile would be generated by exposure to various doses of this genotoxic agent.
2008-04-08 | E-GEOD-7675 | biostudies-arrayexpress
Project description:Early transcriptional responses induced by benzo(a)pyrene diol epoxide in human amnion epithelial FL cells
| PRJNA99729 | ENA
Project description:Genotoxic agents cause cellular DNA damage and stress responses, including transcriptional changes. Here we focused on the early transcriptional responses of human cells to benzo(a)pyrene diol epoxide (BPDE), which causes bulky DNA adduct damage. Human amnion epithelial FL cells were exposed to three doses of BPDE (5, 50, and 500 nM) and the vehicle control DMSO, and differential gene expression profiles were obtained 4 h after exposure using oligonucleotide microarrays followed by validation with quantitative real-time RT-PCR. Compared with a few genes affected by the low and medium-dose exposure, extensive and robust changes in gene expression were induced by the high-dose BPDE. We found that the expression of cell cycle-regulators, signaling molecules and transcription factors were significantly altered and important signaling pathways related to cell survival or apoptosis were affected by BPDE. Several genes and related regulatory pathways that were previously not known to be responsive to this genotoxic agent have now been implicated, which helps to draw the whole picture of how cells respond to environmental chemical exposure via transcriptional regulation. Keywords: Dose response
2008-01-01 | GSE7675 | GEO
Project description:The environmental carcinogen, (±)-anti-benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE), causes bulky-adduct DNA damages, triggers certain signaling pathways, and elicits gene expression changes. Here, we focused on the temporal gene expression changes induced by a low concentration (0.05 µM) BPDE in human amnion epithelial FL cells. Differential gene expression profiles at 1, 10 and 22 h post BPDE treatment were obtained using Affymetrix HG-U133 Plus 2.0 oligonucleotide microarrays. A cohort of gene expression changes related to cell cycle progression, cell growth or apoptosis, stress response, and post-transcriptional regulation was validated with quantitative real-time RT-PCR. The alteration of several cell cycle-related genes was correlated and possibly contributed to the cell cycle arrest phenotype. Paradoxical transcriptional regulations regarding cell growth or apoptosis emerged in response to BPDE treatment, which indicated that cell fate was determined by integrated signals. The temporal transcriptional changes would be of help to clarify the molecular mechanism of cellular response to BPDE. Experiment Overall Design: Human amnion epithelial FL cells were exposed to vehicle control (dimethyl sulfoxide) and a low concentration (0.05 µM) (±)-anti-benzo[a]pyrene-7,8-diol-9,10-epoxide, respectively. The differential gene expression profiles at 1, 10 and 22 h post BPDE treatment were obtained using Affymetrix HG-U133 Plus 2.0 oligonucleotide microarrays. The transcriptomic changes at different time points post BPDE treatment would provide insight into the dynamic processes of cellular response to this genotoxic agent.
2009-01-14 | E-GEOD-10979 | biostudies-arrayexpress
Project description:Genome-wide screening of temporal responsive genes induced by a low concentration of the carcinogen N-methyl-N'-nitro-N-nitrosoguanidine in a normal human cell line
| PRJNA126257 | ENA
Project description:In this work, we generated early human amnion-like tissues by culturing human pluripotent stem cells (hPSCs) in a bioengineered implantation-like niche in vitro. To explore the gene expression profile of hPSC-derived amnion-like cells (hPSC-amnion), we performed mRNA-sequencing for both undifferentiated hPSCs and hPSC-amnion. Here we show that hPSC-amnion differs from hPSCs by actively regulating a comprehensive set of transcriptional regulation network and developmental signaling pathways such as BMP-SMAD signaling.
2016-12-06 | GSE89479 | GEO