제 1 차 유전공학 학술세미나 초록 = The 1th Seminar of the institute of Genetic Engineering

다국어 초록 (Multilingual Abstract)

Exposure to environmental chemicals has been suggested as a risk factor to explain a portion of the incidence of breast cancer. It has been well documented that the presence of organochlorine residues such as DDT and HCH in breast tissues in the United States. The present study was undertaken to investigate whether the action of DDT particularly the most estrogenic o.p-DDT to increase protein phosphorylation activities in cells could be related to activation of any known mitogenic or estrogen-inducible transformational changse in well studied human breast cancer MCF-7 cells. In results, o.p-DDT was found to be potent activator of protein kinases. Among the activated kinases, protein tyrosine kinases appear to be most affected as observed by the antagonistic action of genistein, a well known protein tyrosine kinase inhibitor. Cell free system showed essentially the same trend as the results shown in intact cells. Tamoxifen, a specific blocker of the estrogen receptor did not antagonize the action of o.p-DDT. However, an antibody against e-Neu drastically inhibited the protein tyrosine kinase activity. Genistein was again effective in inhibition of this protein tyrosine activity. As a result of immunoprecipitation with a specific antibody against e-new and protein A-sepharose, we could show that e-Nwe protein is at least one of the protein tyrosine kinases which o.p-DDT activates. Moreover, EGF binding activity to EFG binding activity of nuclear transcription factors, especially the early response gene, e-myc and one of the house keeping gene, SPI were increased depending upon the exposing time by o.p-DDT and Estradiol. These findings together indicated that the action of o.p-DDT is mediated by e-Neu kinase.