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 M) 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.
Temporal gene expression changes induced by a low concentration of benzo[a]pyrene diol epoxide in a normal human cell line.
Sex
View SamplesGenotoxic 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.
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View SamplesThe 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 10.0M),and differential gene expression profiles were obtained 4 h after exposure using oligonucleotide microarrays followed by validation with quantitative real-time RT-PCR.
Identification of early responsive genes in human amnion epithelial FL cells induced by N-methyl-N'-nitro-N-nitrosoguanidine using oligonucleotide microarray and quantitative real-time RT-PCR approaches.
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View SamplesThe prognosis of pancreatic cancer is still very poor, how to detect pancreatic cancer from high-risk group in an early stage is essential for improving its long-time survival. Therefore, the purpose of this study was to explore specific biomarkers that can differentiate pancreatic cancer-associated diabetes from type-2 diabetes for the early detection of pancreatic cancer. In the current study, we used global gene transcription analysis with affymetrix gene chip to identify genes specifically expressed in pancreatic cancer-associated diabetes mellitus from peripheral blood samples in stead of from tissue samples.
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Sex, Age, Disease, Subject
View SamplesIt has been demonstrated that Ring finger protein 43 (RNF43) is overexpressed in colorectal cancer and mediates cancer cell proliferation. We found that RNF43 was frequently overexpressed in HCC, and knockdown of RNF43 could induce apoptosis and inhibit proliferation, invasion, colony formation and xenograft growth of HCC cells. Suggesting that RNF43 is involved in tumorigenesis and progression of HCC.
Reversing effect of ring finger protein 43 inhibition on malignant phenotypes of human hepatocellular carcinoma.
Cell line, Treatment
View SamplesHeat shock proteins are highly conserved proteins that, when produced intracellularly, protect stress exposed cells. It has been suggested that extracellular Hsp70 has both protective and deleterious effects. Our study showed eHSP70 increased the ALP activity, promoted mineralization and up-regulated osteogenesis-related markers.
Extracellular heat shock protein 70 promotes osteogenesis of human mesenchymal stem cells through activation of the ERK signaling pathway.
Sex, Specimen part
View SamplesUnderstanding the interactions of nanostructures with biological systems is essential to nanotoxicological research.
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Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
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Age, Specimen part, Cell line, Treatment
View SamplesPredose and postdose gene expression profiles of blood samples of five most susceptible and five most resistant rats to acetaminophen-induced hapatotoxicity were determined by microarray analysis.
Predose and Postdose Blood Gene Expression Profiles Identify the Individuals Susceptible to Acetaminophen-Induced Liver Injury in Rats.
Sex, Specimen part
View SamplesThe 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 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.
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Sex, Specimen part
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