Cell cycle arrest at M phase induced by vinblastine in MOLT-4 cells.
- Author:
Yi-Sheng ZHONG
1
;
Chang-Chuan PAN
;
Chang-Nan JIN
;
Jian-Jun LI
;
Gong-Peng XIONG
;
Jian-Xi ZHANG
;
Jian-Ping GONG
Author Information
1. Department of Hepatic Surgery, Xiamen Hospital of Traditional Chinese Medicine, Xiamen 361009, Fujian Province, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Cell Cycle;
drug effects;
Cell Division;
drug effects;
Flow Cytometry;
Humans;
Tumor Cells, Cultured;
Vinblastine;
pharmacology
- From:
Journal of Experimental Hematology
2009;17(2):358-362
- CountryChina
- Language:Chinese
-
Abstract:
This study was purposed to investigate the biological effect of vinblastine (VLS), usually known as inductor of mitotic arrest, on MOLT-4 of ALL cells and to evaluate its significance. The cell arrest in M phase and/or cell apoptosis were induced by treatment of MOLT-4 cells with 0.05 microg/ml VLS for 0 - 12 hours; the DNA histogram was detected by flow cytometry; the morphological changes of cells were observed by confocal microscopy; the cell cycle distribution, cell apoptosis and morphological changes of cells before and after arrest were analyzed by using arrest increasing rate (AIR), arrest efficiency (AE), apoptosis rate (AR) and morphologic parameters respectively. The results indicated that the cell arrest did not accompanied by significant increase of apoptosis rate; the DNA histogram of cell arrest showed dynamic change of cell cycle in time-dependent manner; the arrest efficiency could be quantified. The cell arrest at M phase was accompanied by cell stack in S phase, the cell proliferation rate dropped after cell arrest occurred. The cells arrested at M phase possessed of characteristic morphologic features in cell mitosis. It is concluded that the vinblastine can solely induce arrest of MOLT-4 cells at M phase. This study provides experimental basis for further investigating the relation of cell cycle arrest to apoptosis, mechanism of checkpoint and development of new anticancer drugs.
