Mechanism of lithium chloride-induced proliferation inhibition and apoptosis of K562 leukemic cells.
- Author:
Hua-Rong TANG
1
;
Qun HE
;
Fa-Chun WANG
Author Information
1. Centeral Laboratory, Affiliated People's Hospital, Jiangsu University, Zhenjiang 210002, China.
- Publication Type:Journal Article
- MeSH:
Antineoplastic Agents;
pharmacology;
Apoptosis;
drug effects;
Cell Cycle;
drug effects;
Cell Proliferation;
drug effects;
Colforsin;
pharmacology;
Flow Cytometry;
Fusion Proteins, bcr-abl;
genetics;
Gene Expression Regulation, Neoplastic;
drug effects;
Humans;
K562 Cells;
Leukemia;
genetics;
metabolism;
pathology;
Lithium Chloride;
pharmacology;
Potassium Channel Blockers;
pharmacology;
RNA, Messenger;
biosynthesis;
genetics;
Reverse Transcriptase Polymerase Chain Reaction;
Sodium Channel Blockers;
pharmacology;
Tetrodotoxin;
pharmacology
- From:
Journal of Experimental Hematology
2005;13(6):979-982
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the mechanism of proliferation inhibition and apoptosis of K562 leukemia cells by lithium chloride (LiCl), after K562 cells were treated with LiCl (30 mmol/L) cell cycle was examined by flow cytometry (FCM) and the expression of bcr/abl fusion gene mRNA was evaluated by RT-PCR. The intracellular Li(+) concentrations of K562 cells were determined at different time after treated with 30 mmol/L LiCl and the effects of TTX and FSK on intracellular Li(+) concentrations of K562 cells were also detected by atomic absorption spectrometry. The effects of TTX and FSK on LiCl-induced growth inhibition of K562 cells were determined by cell counting in liquid culture. The results showed that LiCl (30 mmol/L) caused a sustained arrest in G(2)/M cell cycle and down-regulated the bcr/abl mRNA expression in K562 cells, the intracellular Li(+) concentration of K562 cells increased at 30 minutes after treated with 30 mmol/L LiCl and reached apex at 2 hours, thereafter, gradually decreased and balanced at 4 hours after the treatment. If either Na(+) channel was pre-blocked with TTX or K(+) channel was pre-blocked with FSK, the intracellular Li(+) concentrations of K562 cells treated with 30 mmol/L LiCl were higher than that in the cells just treated with LiCl without pre-blocking. Furthermore, after pre-blocking either Na(+) channel with TTX or K(+) channel with FSK, the inhibition rate of K562 cell growth by 30 mmol/L LiCl could be increased. It is concluded that the mechanism of proliferation inhibition and apoptosis of K562 leukemia cells induced by LiCl is probably related with the G(2)/M cell cycle arrest, the bcr/abl mRNA expression down-regulation and the status of Na(+), K(+), or Li(+) ion channels on K562 leukemia cells.
