Inhibition of K562 cell proliferation by wild type p16 and p53 genes co-transfection.
- Author:
Hong-Bing RUI
1
;
De-Fu YE
;
Guang-Sheng ZHUO
;
Jun-Min CHEN
;
Yuan XUE
;
Ling ZHENG
;
Yue-Yong ZHU
;
Ri-Hui KANG
;
Jun-Fang LING
Author Information
1. Department of Hematology, The First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China. fjrhb@sina.com
- Publication Type:Journal Article
- MeSH:
Cell Division;
Genes, p16;
physiology;
Genes, p53;
physiology;
Humans;
K562 Cells;
Plasmids;
Transfection
- From:
Journal of Experimental Hematology
2002;10(5):400-403
- CountryChina
- Language: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.
