Effect of honokiol on proliferation and apoptosis in HL-60 cells and its potential mechanism.
10.7534/j.issn.1009-2137.2014.06.015
- Author:
Jia-Xin FAN
1
;
Ying-Jian ZENG
2
;
Guang-Yang WENG
3
;
Jian-Wei WU
1
;
Zhang-Qiu LI
1
;
Yuan-Ming LI
1
;
Rong ZHENG
1
;
Kun-Yuan GUO
3
Author Information
1. Department of Hematology, Wuyi Hospital of Traditional Chinese Medicine/Traditional Chinese Medicine Hospital of Jinan University Medical College, Jiangmen 529000, Guangdong Province, China.
2. Department of Hematology, Wuyi Hospital of Traditional Chinese Medicine/Traditional Chinese Medicine Hospital of Jinan University Medical College, Jiangmen 529000, Guangdong Province, China. E-mail: Zengyingjian1975@163.com.
3. Department of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, Guangdong Province, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Biphenyl Compounds;
pharmacology;
Caspase 3;
Cell Cycle;
Cell Proliferation;
drug effects;
Cyclin D1;
Cyclin E;
Cyclin-Dependent Kinase 2;
HL-60 Cells;
Humans;
Lignans;
pharmacology;
Oncogene Proteins;
Signal Transduction;
bcl-2-Associated X Protein
- From:
Journal of Experimental Hematology
2014;22(6):1577-1583
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to investigate the effect of Honokiol (HNK) on proliferation and apoptosis of acute myeloid leukemia HL-60 cells and its potential mechanism. Inhibitory effect of HNK on the HL-60 cell proliferation was detected by MTT assay. Flow cytometry was used to detect the change of cell cycle and AnnexinV/PI staining was used to detect apoptosis. Western blot was applied to analyze the cell cycle protein (cyclins), cyclin-dependent kinase (CDK), P53, P21, P27, BCL-2, BCL-XL, Bax, caspase-3/9 and proteins for MAPK signal pathway. The results showed that HNK could inhibit the proliferation of HL-60 cells in time- and dose dependent ways. HNK arrested HL-60 cells in G0/G1 phase, and S phase cells decreased significantly (P < 0.05). The expression of cyclin D1, cyclin A, cyclin E and CDK2/4/6 were significantly down-regulated (P < 0.05), the expression of P53 and P21 was significantly upregulated after treating for 24 h with HNK (P < 0.05). After 24 h treatment with HNK, HL-60 cell apoptosis increased significantly with the upregulation of activated caspase-3, -9, BAX expression and the downregulation of BCL-2, BCL-XL expression. The MAPK subfamily, P38 and JNK were not significantly changed, but the expression of MEK1/2-ERK1/2 was significantly downregulated (P < 0.05). It is concluded that HNK arrestes the cells at G0/G1 phase and induces HL-60 cell apoptosis through the intervention of MEK1/2-ERK1/2 signaling pathway.
