Sensitivity of anticancer drugs in Saos-2 cells transfected with mutant p53 varied with mutation point.
A human osteosarcoma cell line, Saos-2, which is devoid of endogenous p53 gene, and clones of Saos-2 cells, which were transfected with wild type p53 or mutant p53 genes (123A, 143A, 175H and 273H), were observed for their surviving fraction after treatment with the commonly used anticancer drugs, cisplatin (CDDP), nimustine (ACNU), adriamicin (ADR) and bleomicin (BLM). The transfectants of the mutant 143A, 175H and 273H were significantly more resistant to CDDP than the transfectant of pOPI3 (expression plasmid only). The transfectants of the wild type p53 and mutant 123A were significantly more sensitive to ACNU than the transfectant of pOPI3. The transfectant of mutant 123A was more sensitive to ADR than the transfectant of pOPI3. There was no significant difference in sensitivity to BLM between Saos-2 and all kinds of transfectants. Thus the sensitivity of the cells to anticancer drugs varied with the mutation point of the p53 gene.
Wang
L H
LH
Department of Radiation Biophysics, Nagasaki University School of Medicine, Japan.
Okaichi
K
K
Ihara
M
M
Okumura
Y
Y
D001761:Bleomycin / Q000627:therapeutic use*; D002945:Cisplatin / Q000627:therapeutic use*; D004317:Doxorubicin / Q000627:therapeutic use*; D019008:Drug Resistance, Neoplasm; D016158:Genes, p53; D006801:Humans; D016297:Mutagenesis, Site-Directed; D015376:Nimustine / Q000627:therapeutic use*; D012516:Osteosarcoma / Q000235:genetics*; D017354:Point Mutation; D014162:Transfection; D014407:Tumor Cells, Cultured; D016159:Tumor Suppressor Protein p53 / Q000502:physiology*
D016159:Tumor Suppressor Protein p53; D015376:Nimustine; D001761:Bleomycin; D004317:Doxorubicin; D002945:Cisplatin