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사람 유래의 MCF10A, Chang liver 및 HaCaT 세포의 소핵형성 및 세포형질전환에 미치는 2,3,7,8-Tetrachlorodibenzo-p-dioxin의 영향
엄미옥(Miok Eom),박미영(Miyoung Park),김종원(Jongwon Kim),박미선(Misun Park),한의식(Euisik Han),오혜영(Hyeyoung Oh),정해관(Haikwan Jung) 한국환경성돌연변이발암원학회 2004 한국환경성돌연변이·발암원학회지 Vol.24 No.2
Although 2,3,7,8-tetrachlorodibenzo-p-dioxin(TCDD) is a powerful carcinogen in several species, limited model system exist to study carcinogenicity of this compound at cellular level. To enhance our understanding of carcinogenicity of TCDD at cellular level, we investigated micronucleus (MN) frequency as a index of genetic toxicity and whether TCDD can transform the human cells in culture. Normal human cell lines, skin keratinocyte HaCaT, Chang liver and breast MCF10A cells were used. TCDD did not affect the cell viability of the Chang liver, HaCaT and MCF10A cells. The frequency of micronucleus was increased after treatment of TCDD for 24hr in Chang liver and HaCaT cells, but not changed in MCF10A cells. And we observed putative transformed cells in Chang liver cells exposed to 1μM TCDD for 2 weeks. The putative transformed cells were also observed in HaCaT cells with subsequent exposure to TCDD (0.1, 1, 10, 100 nM) for 2 weeks after initial exposure to MNNG, but not observed in MCF10A cells. Collectively, these results indicate that the ability of TCDD to induce micronuclei may be involved in cellular transformation of Chang liver and HaCaT cells. Our putative TCDD-transformed cells of Chang liver and HaCaT are expected to provide a clue to the elucidation of TCDD-induced transformation pathway.
폐암세포주에서 아데노바이러스 매개 p16 유전자 전달로 인한 유전자 발현의 변화
박미선(Misun Park),김옥희(Okhee Kim),박현신(Hyunshin Park),지승완(Seungwan Jee),엄미옥(Miok Eom),엄태경(Taikyung Ryeom),강호일(Hoil Kang) 한국독성학회 2004 Toxicological Research Vol.20 No.1
For the safety evaluation of adenovirus-mediated gene transfer, we investigated differential gene expressions after transfecting adenoviral vector containing p16 tumor suppressor gene (Ad5CMV-p16) into human non-small cell lung cancer cells. In the previous study, we showed adenovirus-mediated p16INK4a gene transfer resulted in significant inhibition of cancer cell growth. We investigated gene expression changes after transfecting Ad5CMV-p16, Ad5CMV (null type, a mock vector) into A549 cells by using cDNA chip and oligonucleotide microarray chip (1200 genes) which carries genes related with signal transduction pathways, cell cycle regulations, oncogenes and tumor suppressor genes. We found that p16INK4a gene transfer down regulated 5 genes (cdc2, cyclin D3, cyclin B, cyclin E, cdk2) among 26 genes involved in cell cycle regulations. Compared with serum-free medium treated cells, Ad5CMV-p16 changed 27 gene expressions, two fold or more on oligonucleotide chip. In addition, Ad5CMV-p16 did not seem to increase the tumorigenicity-related gene expression in A549 cells. Further studies will be needed to investigate the effect of Ad5CMV-p16 on normal human cells and tissues for safety evaluation.
폐암세포주에서 아데노바이러스 매개 p16 유전자 전달로 인한 유전자 발현의 변화
박미선(Misun Park),김옥희(Okhee Kim),박현신(Hyunshin Park),지승완(Seungwan Jee),엄미옥(Miok Eom),염태경(Taikyung Ryeom),강호일(Hoil Kang) 한국독성학회 2004 Toxicological Research Vol.20 No.2
For the safety evaluation of adenovirus-mediated gene transfer, we investigated differential gene expressions after transfecting adenoviral vector containing p16 tumor suppressor gene (Ad5CMV-p16) into human non-small cell lung cancer cells. In the previous study, we showed adenovirus-mediated p16INK4a gene transfer resulted in significant inhibition of cancer cell growth. We investigated gene expression changes after transfecting Ad5CMV-p16, Ad5CMV (null type , a mock vector) into A549 cells by using cDNA chip and <br/> oligonucleotide microarray chip (1200 genes) which carries genes related with signal transduction pathways, cell cycle regulations, oncogenes and tumor suppressor genes. We found that p16INK4a gene transfer down regulated 5 genes (cdc2, cyclin D3, cyclin B, cyclin E, cdk2) among 26 genes involved in cell cycle regulations. Compared with serum-free medium treated cells, Ad5CMV-p16 changed 27 gene expressions, two fold or more on oligonucleotide chip. In addition, Ad5CMV-p16 did not seem to increase the tumorigenicity-related gene expression in A549 cells. Further studies will be needed to investigate the effect of Ad5CMV-p16 on normal human cells and tissues for safety evaluation.
지승완(Seungwan Jee),김창환(Changhwan Kim),박미선(Misun Park),엄미옥(Miok Eom),염태경(Taikyung Ryeom),김옥희(Okhee Kim),강호일(Hoil Kang) 한국독성학회 2005 Toxicological Research Vol.21 No.1
Chrysin (5,7-dihydroxyflavone) is a flavonoid compound contained in many fruits, vegetables and honey. In our experiment, we investigated genotoxicity of chrysin using bacterial reverse mutation assay, chromosomal aberration test, in vivo micronucleus test. In bacterial reverse mutation assay, chrysin did not induce mutagenicity in Salmonella typhimurium TA98, TA100, TA1535, TA1537, TA102 with and without metabolic activation. In chromosome aberration test, chrysin did not also induce structural and numerical abberations regardless of metabolic activation in Chinese hamster lung fibroblast cells. In mouse micronucleus test, no significant increase in the occurrence of micronucleated polychromatic erythrocytes (MNPCE) was observed in ICR male mice orally administered with chrysin at the dose of 0.5, 1.0, 2.0 g/kg body weight. Taken together these results, chrysin has no mutagenic potential in our experiment.