Effect of microRNA-17-92 cluster on the biological characteristics of K562 cells and its mechanisms.
10.7534/j.issn.1009-2137.2014.01.005
- Author:
Shuang YANG
1
,
2
;
Hui-Yan SUN
3
;
Feng-Jun XIAO
3
;
Qing-Fang LI
4
;
Jun XU
3
;
Zi-Kuan GUO
3
;
Heng-Xiang WANG
5
;
Li-Sheng WANG
3
Author Information
1. Department of Hematology, Dalian Medical University, Dalian 116044, Liaoning Province, China
2. Department of Hematology, General Hospital of Chinese Air Force, Beijing 1000142, China.
3. Department of Experimental Hematology, Institute of Radiation Medicine, Academy of Military Medical Sciences, Beijing 100850, China.
4. Cancer Center, Chinese PLA General Hospital, Beijing 100853, China.
5. Department of Hematology, General Hospital of Chinese Air Force, Beijing 1000142, China. E-mail:wanghengxiang123@yahoo.com.cn.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Cell Cycle;
Cell Proliferation;
Gene Expression Regulation, Leukemic;
HL-60 Cells;
Humans;
K562 Cells;
Leukemia, Myelogenous, Chronic, BCR-ABL Positive;
genetics;
metabolism;
MicroRNAs;
genetics;
Transfection
- From:
Journal of Experimental Hematology
2014;22(1):20-24
- CountryChina
- Language:Chinese
-
Abstract:
The objective of this study was to explore the effects of microRNA-17-92 on the biological characteristics of K562 cells. The expression of miR-17-92 in K562 cells transfected with miRNA-17-92 mimic was detected by real time PCR. The effect of microRNA-17-92 on K562 cell proliferation was detected by CCK-8 method. Apoptosis of K562 cells was detected by Annexin V-PI labeling. Cell cycle distribution was determined by using flow cytometry. Western blot was performed to determine the protein levels of Crk. The results indicated that the transfection with miR-17-92 mimic increased expression of mature miR-17-92 in K562 cells. Compared with control group, cell proliferation and cell amount in S-phase of miR-17-92 mimic transfected group significantly increased, cell apoptosis decreased. The expression of signal connector protein Crk was greatly up-regulated in miR-17-92-mimic-transfected K562 cells. It is concluded that miR-17-92 can promote proliferation, inhibit apoptosis and regulate the cell cycle of K562 cells.
