Differential Gene Expression Induced by Naphthalene in Two Human Cell Line, HepG2 and HL-60

Authors
Kim, Youn-JungSong, MeeSong, Mi-KyungYouk, Da-YoungChoi, Han-SaemSarma, Sailendra NathRyu, Jae-Chun
Issue Date
2009-06-30
Publisher
KOREAN SOCIETY TOXICOGENOMICS & TOXICOPROTEOMICS-KSTT
Citation
MOLECULAR & CELLULAR TOXICOLOGY, v.5, no.2, pp.99 - 107
Abstract
Naphthalene is bicyclic aromatic compound that is widely used in various domestic and commercial applications including lavatory scent disks, soil fumigants and moth balls. Exposure to naphthalene results in the development of bronchiolar damage, cataracts and hemolytic anemia in humans and laboratory animals. However, little information is available regarding the mechanism of naphthalene toxicity. We investigated gene expression profiles and potential signature genes in human hepatocellular carcinoma HepG2 cells and human promyelocytic leukemia HL-60 cells after 3 h and 48 h incubation with the IC20 and IC50 of naphthalene by using 44 k agilent whole human genome oligomicroarray and operon human whole 35 k oligomicroarray, respectively. We identified 616 upregulated genes and 2,088 down-regulated genes changed by more than 2-fold by naphthalene in HepG2 cells. And in HL-60, we identified 138 up-regulated genes and 182 down-regulated genes changed by more than 2-fold. This study identified several interesting targets and functions in relation to naphthalene-induced toxicity through a gene ontology analysis method. Apoptosis and cell cycle related genes are more commonly expressed than other functional genes in both cell lines. In summary, the use of in vitro models with global expression profiling emerges as a relevant approach toward the identification of biomarkers associated with toxicity after exposure to a variety of environmental toxicants.
Keywords
INDUCED OXIDATIVE STRESS; GLUTATHIONE DEPLETION; DNA-DAMAGE; TOXICITY; PROLIFERATION; INDUCED OXIDATIVE STRESS; GLUTATHIONE DEPLETION; DNA-DAMAGE; TOXICITY; PROLIFERATION; Naphthalene; HepG2; HL-60; Gene ontology; Differentially expressed gene (DEG)
ISSN
1738-642X
URI
https://pubs.kist.re.kr/handle/201004/132382
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KIST Article > 2009
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