[Wild-type p53 stimulates vincristine-induced apoptosis]

Yao Xue Xue Bao. 1997 Aug;32(8):565-8.
[Article in Chinese]

Abstract

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.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents, Phytogenic / pharmacology
  • Apoptosis / drug effects*
  • Drug Resistance, Neoplasm / genetics
  • Genes, p53*
  • Humans
  • KB Cells
  • Vincristine / pharmacology*

Substances

  • Antineoplastic Agents, Phytogenic
  • Vincristine