| Objective:Prepared by recombinant antisense c-myc and identification of adenovirus and transfected osteosarcoma MG-63 cells (P53-deficient) and U2OS cells (P53 wild type), Through more than two osteosarcoma cells c-myc antisense recombinant adenoviral gene interference after osteosarcoma cells with low expression c-myc, and then by using different concentrations of cisplatin at different times, cisplatin for osteosarcoma the impact of apoptosis.Methods:After the reorganization of c-myc antisense adenovirus in vitro transfection MG-63 cells and U2OS cell 12h,24h,48h after c-myc antisense adenovirus (Ad-Asc-myc), c-myc gene expression assay and after c-my protein expression was measured in vitro infection of human osteosarcoma MG-63 cells and U2OS cells with a concentration of 2.0,5.0μg/cisplatin ml of 2h, 4h,8h after using Western blot (Western blot) method for detecting the level of interference; osteosarcoma cells through Wright’s staining and MTT assay, testing different concentrations of morphological and statistical cisplatin low expression of c-myc in the role of MG-63 cells and U2OS apoptosis.Results:Build package adenovirus Ad-Asc-myc in vitro infection MG-63 cells and U2OS cells after 48h, can significantly reduce the expression levels of c-myc osteosarcoma cell protein; at the same time, cisplatin low c-myc expression in osteosarcoma MG-63 cells and U2OS cell line were significantly enhanced.Conclusion:Inhibit the expression of c-myc osteosarcoma cell osteosarcoma can enhance the sensitivity of cisplatin, but with cisplatin concentration and reaction time was no obvious meaning. |
