摘要
In order to explore whether the protective function of GST-pi can prevent transformation in vitro, NIH3T3 cells and carcinogen glycidyl methacrylate (GMA) have been used in cell transformation study. NIH3T3 cells have been transfected with GST-pi cDNA inserted retrovirus vector, pXT1, and then G418 resistant clones have been analyzed by Southern and Northern analyses. NIH3T3/pXGST clones that stably express GST-pi and control cells,
In order to explore whether the protective function of GST-pi can prevent transformationin vitro, NIH3T3 cells and carcinogen glycidyl methacrylate (GMA) have been used in cell transformation study. NIH3T3 cells have been transfected with GST-pi cDNA inserted retrovirus vector, pXT1, and then G418 resistant clones have been analyzed by Southern and Northern analyses. NIH3T3/pXGST clones that stably express GST-pi and control cells, untransfected NIH3T3 and NIH3T3/pXT1, have been treated three times discontinuously with GMA. 1.287% of untransfected NIH3T3 and 1.197% of NIH3T3/pXT1, cells obtained a transformation phenotype, forming type III transformed clones, which could grow in soft agar and form fibrosarcoma in nude mice. In comparison, the transformation rate is only 0.007% in NIH3T3/pXGST cells, which could not grow in soft agar and formed no tumorin vivo. The results showed that expression of exogenous GST-pi in NIH3T3 do protect NIH3T3 cells from GMA induced transformationin vitro, which provides an evidence that GST-pi may play a role In preventing chemical carcinogenesis.
