Effect of SU11248 on leukemia cell line K562 and its molecular mechanisms.
10.7534/j.issn.1009-2137.2014.04.015
- Author:
Ling-Qing LUO
1
;
Xiao CHENG
2
;
Yan CHEN
1
;
Zhao-Lei CUI
3
;
Dong-Hong LIN
4
Author Information
1. Department of Laboratorial Examination, Fujian Tumor Hospital of Fujian Medical University Teaching Hospital, Fuzhou 350014, Fujian Province, China.
2. Department of Cardiovasology, Fujian Mindong Hospital Affiliated to Fujian Medical University, Fu'an 355000, Fujian Province, China.
3. Department of Laboratorial Examination, College of Medical Technology and Engineering, Fujian Medical University, Fuzhou 350004, Fujian Province, China.
4. Department of Laboratorial Examination, College of Medical Technology and Engineering, Fujian Medical University, Fuzhou 350004, Fujian Province, China. E-mail:lindh65@163.com.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Cell Proliferation;
drug effects;
Fusion Proteins, bcr-abl;
metabolism;
Humans;
Indoles;
pharmacology;
K562 Cells;
Proto-Oncogene Proteins c-akt;
metabolism;
Proto-Oncogene Proteins c-myc;
metabolism;
Pyrroles;
pharmacology;
RNA, Messenger;
genetics;
Telomerase;
metabolism
- From:
Journal of Experimental Hematology
2014;22(4):965-970
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to investigate the effect of SU11248 on proliferation and apoptosis of leukemia cell line K562 in vitro and its mechanism. The inhibitory effect of 3.2 µg/ml SU11248 on K562 proliferation was tested by MTT assay. The ability of SU11248 to induce apoptosis of K562 cells was examined by TUNEL and DNA ladder. The expression of C-MYC, hTERT and BCR-ABL mRNA in K562 cells was detected by RT-PCR. The protein expression of Akt and p-Akt in K562 cells was detected by Western blot. The results showed that the proliferation of K562 cells was obviously inhibited by 3.2 µg/ml SU11248 in a time-dependent manner. SU11248 could induce K562 cells apoptosis in dose-and time-dependent manner. The mRNA expression of C-MYC, hTERT and BCR-ABL was reduced significantly by SU11248 in a time-dependent manner (P < 0.05). Western blot detection showed that the expression of p-Akt protein in K562 cells decreased in dose-and time-dependent manner after SU11248 treatment, but the expression of Akt was not significantly changed. It is concluded that SU11248 can inhibit the growth of K562 cells efficiently through inducing apoptosis, its mechanism may be closely relate with the expression down-regulation of C-MYC, hTERT, BCR-ABL and the inhibition of Akt phosphorylation.
