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To evaluate the effects of wild type p53 gene on the growth and chemotherapeutic sensitivity of human glioma cells, plasmid PC53 SN3 carrying wild type p53 gene was transfected into U251 cells. p53 gene expression in transfected cells was detected by RT PCR, the cell growth inhibition and apoptosis in either the absence or the presence of cisplatin was assessed by MTT and flow cytometry. The transfection of p53 gene into U251 cells was confirmed by RT PCR. MTT showed that p53 gene by itself induced strong inhibition effect on the growth of U251 cells [inhibition rate, IR (79.60±5.69) %]. The killing effects of cisplatin by itself on U251 cells was not strong [IR (19.40±6.69) %, (24.41±2.68) %, (51.84±13.38) %, (66.22±5.02) %] and increased with the increase of cisplatin concentration (1, 2, 4, 8 μg/ml). When combined treatment of wild type p53 gene transfection and cisplatin was used, that was significantly increased [IR (91.64±1.00) %, (94.98±1.67) %, (95.32±2.01)%, (95.65±1.00) %]. The apoptosis rate of U251 cells induced by p53 gene transfection was 17.38%. That induced by cisplatin increased (5.71 %, 5.93 %, 6.27 %, and 6.81 %) with the increase of cisplatin concentration (1, 2, 4, 8 μg/ml). The apoptosis rate was also significantly increased (23.50 %, 23.54 %, 23.89 %, and 28.88 %) after combined treatment of p53 and cisplatin with different concentration (1, 2, 4, 8 μg/ml). It is concluded that wild type p53 gene and cisplatin could result in synergistic inhibition effects on the growth of human glioma cells.
To evaluate the effects of wild type p53 gene on the growth and chemotherapeutic sensitivity of human glioma cells, plasmid PC53 SN3 carrying wild type p53 gene was transfected into U251 cells. P53 gene expression in transfected cells was detected by RT PCR, the cell growth inhibition and apoptosis in either the absence or the presence of cisplatin was assessed by MTT and flow cytometry. The transfection of p53 gene into U251 cells was confirmed by RT PCR. MTT showed that p53 gene by itself induced strong inhibition effect on the growth of U251 cells The killing effects of cisplatin by itself on U251 cells was not strong [IR (19.40 ± 6.69)%, (24.41 ± 2.68)%, (51.84 ± 13.38)%, ( 66.22 ± 5.02)%] and increased with the increase of cisplatin concentration (1, 2, 4, 8 μg / ml). When combined treatment of wild type p53 gene transfection and cisplatin was used, that was significantly increased [IR (91.64 ± 1.00)%, (94.98 ± 1.67)%, (95.32 ± 2.01)%, (95 .65 ± 1.00)%]. The apoptosis rate of U251 cells induced by p53 gene transfection was 17.38%. That induced by cisplatin increased (5.71%, 5.93%, 6.27%, and 6.81%) with the increase of cisplatin concentration , 2, 4, 8 μg / ml). The combined apoptosis rates were also significantly increased (23.50%, 23.54%, 23.89%, and 28.88%) after combined treatment of p53 and cisplatin with different concentration (1, 2, 4, 8 μg / ml). It is that that wild type p53 gene and cisplatin could result in synergistic inhibition effects on the growth of human glioma cells.