[Wild-type p53 stimulates vincristine-induced apoptosis].
Recent studies indicate that wild-type p53 can trigger cell apoptosis induced by many chemotherapeutic agents which induce DNA damage or cause disruptions of DNA metabolism, such as ADM, 5-FU, VP-16 and radiation. We introduced the wild-type p53 gene into a MDR cell line KBV200 in which the endogenous p53 was found to be rearranged. By G418 selection and Northern blot analysis, a G418-resistant clone named KBV200-p53 was obtained which continuously expressed the exogenous wild-type p53 mRNA. After treatment with Vincristine(VCR), the wild type p53-expression cells presented typical morphology characteristic of apoptosis analysed under electron and fluorescence microscopes. Flow cytometer analysis showed that the KBV200-p53 cells were more readily undergo apoptosis than their parental cells KBV200. After treatment with VCR 600 nmol.L-1 for 24 h, the apoptotic percentage of KBV200-p53 and KBV200 cells was about 42.4% and 8.4%, respectively. This result indicates that wild-type p53 stimulates VCR-induced apoptosis in KBV200 cells.
Li
Z H
ZH
Cancer Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021.
Zhu
Y J
YJ
Chao
L S
LS
Li
X T
XT
D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D019008:Drug Resistance, Neoplasm / Q000235:genetics; D016158:Genes, p53; D006801:Humans; D007624:KB Cells; D014750:Vincristine / Q000494:pharmacology*
D000972:Antineoplastic Agents, Phytogenic; D014750:Vincristine