Inability to induce the alteration of tumorigenicity and chemosensitivity of p53-null human pancreatic carcinoma cells after the transduction of wild-type p53 gene

Anticancer Res. Mar-Apr 1997;17(2A):879-83.

Abstract

We investigated the therapeutic benefits of p53 expression by the transduction of wild-type p53 gene into p53-null human pancreatic carcinoma cells (AsPC-1). Induction of p21WAF1/CIP1 protein was observed in p53 gene-transduced AsPC-1 cells, showing the proper function of integrated p53 gene. However, the cell growth in vitro of transduced cells was not different from that of parent cells, and the tumor growth of transduced cells inoculated into nude mice was unchanged compared with that of wild-type cells. Moreover, the in vitro sensitivity to 4 different kinds of anticancer agents including cisplatin, etoposide, 5-fluorouracil and paclitaxel, was not modulated by the expression of wild-type p53 gene. Thus, the data presented here suggest that the expression of wild-type p53 gene in p53-null tumor cells does not consistently produce the therapeutic effects previously reported.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Division
  • Genes, p53 / physiology*
  • Genetic Therapy
  • Humans
  • Mice
  • Mice, Inbred BALB C
  • Pancreatic Neoplasms / drug therapy*
  • Pancreatic Neoplasms / genetics
  • Tumor Cells, Cultured