Ontology highlight
ABSTRACT:
PROVIDER: PRJNA923732 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23081756_1.fastq.gz | Fastqsanger.gz | |||
| SRR23081756_2.fastq.gz | Fastqsanger.gz | |||
| SRR23081757_1.fastq.gz | Fastqsanger.gz | |||
| SRR23081757_2.fastq.gz | Fastqsanger.gz | |||
| SRR23081758_1.fastq.gz | Fastqsanger.gz |
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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. Keywords: Dose response
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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 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
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