[Inhibition of K562 cell proliferation by wild type p16 and p53 genes co-transfection]

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2002 Oct;10(5):400-3.
[Article in Chinese]

Abstract

The tumor suppressor gene p53 and p16, both of which play an important role in inhibition of tumorigenesis, are homozygously deleted in human myeloid leukemia cell line K562. To explore the inhibition of K562 cell proliferation by wild type p16 and p53 genes, both p16 and p53 genes were co-transfected into K562 cells mediated by liposome. The expression of the two genes was measured by immunocytochemical method, the cell cycle was analysed by flow cytometry, and the number of recovered viable cells was assessed after transfection. After co-transfection, the p53 and p16 positive cells were 23% and 28%, respectively. The results showed that co-transfection of p16 and p53 genes significantly inhibits cell proliferation comparing with transfection either by p16 gene or by p53 gene (P < 0.05). Expression of p16 and p53 proteins increased the cell number in G(1) phase but decreased the cell number in S phase. It is concluded that co-transfection of p16 and p53 genes has a stronger growth-inhibitory effect on K562 cell growth than that of transfection only by p16 gene or by p53 gene, may be a pathway for gene therapy in leukemia.

Publication types

  • English Abstract

MeSH terms

  • Cell Division
  • Genes, p16 / physiology*
  • Genes, p53 / physiology*
  • Humans
  • K562 Cells
  • Plasmids
  • Transfection