Genome-wide Identification of Ethylbenzene and Trichloroethylene-regulated Genes in Human Promyelocytic Leukemia HL-60 Cells

Title
Genome-wide Identification of Ethylbenzene and Trichloroethylene-regulated Genes in Human Promyelocytic Leukemia HL-60 Cells
Authors
샤르마송미Youn-Jung Kim류재천
Keywords
Ethylbenzene; Trichloroethylene; Gene expression profiles; Gene ontology; KEGG pathway
Issue Date
2011-01
Publisher
BioChip Journal
Citation
VOL 5, NO 1, 19-26
Abstract
Ethylbenzene (EBZ) and trichloroethylene (TCE), the volatile organic compounds (VOCs) are common constituents of cleaning and degreasing agents, paints, pesticides, personal care products, gasoline and solvents. They are the most common waste chemicals from industry. EBZ is classified as a possible carcinogen and TCE is also classified as a probable carcinogen. This study analyzed the genome-wide expression profiles of human promyelocytic leukemia HL-60 cells exposed to EBZ and TCE using a 35-K whole human genome oligonucleotide microarray. Exposure to EBZ and TCE altered the expression of 106 and 332 up- and also 171 and 856 down-regulated genes individually, 44 genes were up-regulated, and 81 common genes were down-regulated. Genes with a significantly increased expression levels (over 1.5 fold and p-values <0.05) with EBZ and TCE were then classified with gene ontology (GO) and KEGG pathway annotation. Clustering of differentially expressed common genes were associated with RIG-Ilike receptor signaling pathway, cytokine-cytokine receptor interaction, toll-like signaling pathway, and small cell lung cancer. GO analysis showed that the major categories in the biological process ontology were immune response, regulation of apoptosis, regulation of programmed cell death, regulation of cell death, and defense response ontology. Functionally important immune response and apoptosis related genes were also validating their expression profiles by quantitative real-time RT-PCR. Thus, this study may provides a valuable information to do further analysis to explore the mechanism of EBZ and TCE induced hematotoxicity.
URI
http://pubs.kist.re.kr/handle/201004/40754
ISSN
1976-0280
Appears in Collections:
KIST Publication > Article
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