Effects of advanced glycosylation end products and tetrandrine on proliferation of K562 and K562/A02 cells.
- Author:
Tian-Tian WANG
1
;
Dan YAN
;
Bao-An CHEN
;
Jian WANG
;
Guo-Hua XIA
;
Shuai WANG
;
Jian CHENG
;
Jia-Hua DING
;
Wen BAO
Author Information
1. Department of Hematology and Oncology, Southeast University Medical College, Jiangsu Province, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Benzylisoquinolines;
pharmacology;
Cell Proliferation;
drug effects;
Gene Expression Regulation, Leukemic;
Glycation End Products, Advanced;
pharmacology;
Humans;
K562 Cells;
Receptor for Advanced Glycation End Products;
metabolism
- From:
Journal of Experimental Hematology
2012;20(2):246-251
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to investigate the effect of advanced glycosylation end products (AGE) on the proliferation of K562 and K562/A02 cells, the effect of tetrandrine (Tet) on proliferation of K562 and K562/A02 cells induced by AGE, and their mechanisms. The effects of AGE on proliferation of K562 and K562/A02 cells and Tet on the proliferation of AGE-induced K562 and K562/A02 cells were assayed by CCK8 kit, the apoptosis rate and the expression of receptor of advanced glycosylation end products (RAGE) in K562 and K562/A02 cells were determined by flow cytometry, the expression of RAGE mRNA was detected by semi-quantitative RT-PCR. The results showed that AGE could promote the proliferation of K562 and K562/A02 cells in a concentration-dependent manner, the cell proliferation was enhanced with time increasing in 0 - 48 h, and was higher than control group after 72 h. AGE up-regulated the RAGE mRNA and protein expressions of K562 and K562/A02 cells in a concentration-dependent manner. Treatment of Tet combined with AGE for 48 h could inhibit the proliferation of K562 and K562/A02 cells promoted by AGE in a concentration-dependent manner, which probably by inducing cell apoptosis, however, there was no obvious effect in the up-regulating expression of RAGE mRNA and protein induced by AGE. It is concluded that AGE can promote the proliferation of K562 and K562/A02 cells, which is probably induced by up-regulating the expression of RAGE mRNA and protein. Tet can inhibit the proliferation of K562 and K562/A02 cells induced by AGE, and the mechanism may be not closely associated with changes of the up-regulating expression of RAGE mRNA and protein induced by AGE.
