Possible mechanism underlying apoptotic induction effect of vitamin K2 on human MDS cell line MUTZ-1.
- Author:
Bao-An CHEN
1
;
Ze-Ye SHAO
;
Guo-Hua XIA
;
Xin XU
;
Jia-Hua DING
;
Chong GAO
;
Yun-Yu SUN
;
Xue-Zhi GAO
Author Information
1. Department of Hematology, Affiliated Zhongda Hospital, Southeast University, Institute of Myelodysplastic Syndrome, Nanjing 210009, China. cba8888@hotmail.com
- Publication Type:Journal Article
- MeSH:
Antineoplastic Agents;
pharmacology;
Apoptosis;
drug effects;
Caspase 3;
metabolism;
Cell Line, Tumor;
Humans;
Inhibitor of Apoptosis Proteins;
Microtubule-Associated Proteins;
biosynthesis;
genetics;
Myelodysplastic Syndromes;
drug therapy;
pathology;
Neoplasm Proteins;
biosynthesis;
genetics;
Proto-Oncogene Proteins c-bcl-2;
biosynthesis;
genetics;
RNA, Messenger;
biosynthesis;
genetics;
Vitamin K 2;
pharmacology;
bcl-2-Associated X Protein;
biosynthesis;
genetics
- From:
Journal of Experimental Hematology
2007;15(1):91-94
- CountryChina
- Language:Chinese
-
Abstract:
The study was aimed to investigate the possible mechanism of vitamin K(2) (VK(2)) on myelodysplastic syndrome (MDS) cell line MUTZ-1 in vitro. The flow cytometry was used to analyze apoptosis rate and the change of cell cycle. The expression of apoptosis-related genes bcl-2, survivin and bax were detected by reverse transcription-polymerase chain reaction (RT-PCR). The activity of caspase-3 was detected by chemiluminescence assay. The results indicated that the apoptosis peak on FCM and positive Annexin-V FITC on cell membrane showed that VK(2) induced apoptosis of MUTZ-1 cells in a dose-and-time-dependent manner, S and G(2) cell decrement, G(0)/G(1) cell arrest, VK(2) significantly down-regulated the expression of bcl-2 and survivin, but had no effect on the expression of bax, the activity of caspase-3 was significantly increased. It is concluded that VK(2) induces apoptosis of MUTZ-1 cells through activating caspase-3 pathways and the apoptosis-related genes bcl-2 and survivin may play important roles in the process of apoptosis induction.
