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Exogenous mutant p53 DNA enhanced cisplatin-induced apoptosis in TSGH-8301 human bladder cancer cells

F L Chang1, Y F Ling, M D Lai

  • 1Department of Biochemistry, College of Medicine, National Cheng Kung University, Tainan, Taiwan, Republic of China.

Anticancer Research
|April 19, 2000
PubMed
Abstract

Insights

The tumor suppressor gene p53 enhances cisplatin-induced apoptosis in bladder cancer cells. Even without mutant p53 expression, wild-type p53 stabilization increases cancer cell sensitivity to chemotherapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The role of tumor suppressor gene p53 in bladder cancer cell apoptosis remains unclear.
  • Investigating the necessity of p53 for cisplatin-induced apoptosis in human bladder cancer cell line TSGH-8301.

Purpose of the Study:

  • To determine the role of wild-type p53 in mediating apoptosis.
  • To understand the effect of mutant p53 expression on bladder cancer cell sensitivity to cisplatin.

Main Methods:

  • TSGH-8301 cells with wild-type p53 were transfected with mutated p53 cDNA.
  • Stable transfectants were confirmed using Southern and Western blotting.
  • Cellular response to cisplatin was assessed via viability, DNA fragmentation, and nuclear condensation assays.

Main Results:

  • Cells with exogenous mutant p53 showed increased cisplatin sensitivity and apoptosis.
  • No significant difference in sensitivity was observed in clones with rearranged or undetectable mutant p53.
  • RT-PCR sequencing revealed no exogenous mutant p53 mRNA expression in transfectants.

Conclusions:

  • Transfectants lost mutant p53 expression but enhanced wild-type p53 expression, conferring cisplatin sensitivity.
  • Transient mutant p53 expression may lead to irreversible p53 stabilization and increased steady-state p53 levels.

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