Effect of honokiol on proliferation and apoptosis in HL-60 cells and its potential mechanism / 中国实验血液学杂志
Journal of Experimental Hematology
; (6): 1577-1583, 2014.
Article
in Zh
| WPRIM
| ID: wpr-340455
Responsible library:
WPRO
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.
Full text:
1
Index:
WPRIM
Main subject:
Pharmacology
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Biphenyl Compounds
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Signal Transduction
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Cell Cycle
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Apoptosis
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Oncogene Proteins
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Lignans
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HL-60 Cells
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Cyclin D1
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Cyclin E
Limits:
Humans
Language:
Zh
Journal:
Journal of Experimental Hematology
Year:
2014
Type:
Article