Inhibition effect of vitamin K2 on human MDS-JSN04 cell line and its possible mechanism.
- Author:
Ze-Ye SHAO
1
;
Bao-An CHEN
;
Jia-Hua DING
;
Guo-Hua XIA
;
Huai-Gang ZHU
;
Xue-Zhi GAO
Author Information
1. Department of Laboratory Examination, College of Clinical Medicine, Southeast University, Nanjing 210009, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
CD11b Antigen;
analysis;
CD13 Antigens;
analysis;
Caspase 3;
metabolism;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Flow Cytometry;
Gene Expression Regulation, Neoplastic;
Humans;
Inhibitor of Apoptosis Proteins;
Luminescent Measurements;
methods;
Microscopy, Electron, Transmission;
Microtubule-Associated Proteins;
genetics;
Myelodysplastic Syndromes;
genetics;
metabolism;
pathology;
Neoplasm Proteins;
genetics;
Proto-Oncogene Proteins c-bcl-2;
genetics;
Reverse Transcriptase Polymerase Chain Reaction;
methods;
Vitamin K 2;
pharmacology;
bcl-2-Associated X Protein;
genetics
- From:
Journal of Experimental Hematology
2005;13(6):1028-1032
- CountryChina
- Language:Chinese
-
Abstract:
To study the effects and possible mechanism of Vitamin K(2) (VK(2)) in the treatment of MDS-JSN04 cells, the changes of morphologic features of MDS-JSN04 cells were investigated by cytomorphology, the apoptosis of MDS-JSN04 cells was observed by transmission electron microscope; cellular proliferation was determined by the MTT assay; cell apoptosis, cell cycle shift and expression of myeloid-specific differentiation antigen (CD11b, CD13) were analyzed by flow cytometry (FCM). The expression of apoptosis-related genes bcl-2, survivin and bax were detected by retrotranscriptase polymerase chain reaction (RT-PCR); the activity of caspase-3 was determined by chemiluminescence assay. The results showed that the typical apoptotic morphological features appeared in cells treated with VK(2) for 72 hours; VK(2) induced apoptosis of MDS-JSN04 cells and in a dose-and-time-dependent manner, G(0)/G(1) cell arrest and significantly down-regulated the expression of bcl-2 and survivin, but had no effect on the expression of bax; the activity of caspase-3 significantly increased. It is concluded that VK(2) induces apoptosis of MDS-JSN04 cells through activating caspase-3 pathways and the apoptosis-related genes bcl-2, survivin may play an important role in this process.
