Effect of CPEB4 on Proliferation and Apoptosis of Chronic Myeloid Leukemia Cells / 中国实验血液学杂志
Journal of Experimental Hematology
;
(6): 1779-1785, 2019.
Article
in Chinese
| WPRIM
| ID: wpr-781397
ABSTRACT
OBJECTIVE@#To explore the expression of CPEB4 in K562 cells, the biological activity and its possible molecular mechanisms.@*METHODS@#Western blot was used to detect the expression of CPEB4 in normal leukocytes and K562 cells. The overexpression plasmid pcDNA3.1(+)-His-CPEB4 and the silencing plasmid pPLK+Puro-CPEB4 shRNA were transfected into K562 cells to change the expression of CPEB4 in K562 cells, and the transfection efficiency was detected by Western blot. Finally, CCK-8 and flow cytometry were used to detect the proliferation and apoptosis of differently treated cells, and the expression changes of proliferation and apoptosis marker proteins (AKT, p-AKT, caspase-3, BCL-2) were detected by Western blot.@*RESULTS@#Compared with normal leukocytes, the expression of CPEB4 protein in K562 cells was higher (P<0.01). Compared with the control group, the proliferation of CPEB4-silenced K562 cells significantly increased (P<0.01), the number of apoptotic cell significantly decreased, and expression of AKT, p-AKT and BCL-2 was significantly increased, the protein expression of caspase-3 was significantly reduced. The proliferation of K562 cells after CPEB4 overexpression was slowed down (P<0.05), the number of apoptotic cells significantly increased,the expressions of AKT, p-AKT and BCL-2 were significantly down-regulated, and the expression of caspase-3 was up-regulated.@*CONCLUSION@#CPEB4 can inhibit the proliferation and promote the apoptosis of K562 cells, the AKT, p-AKT, BCL-2 and caspase-3 are involved in the regulation mechanism.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Transfection
/
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
/
RNA-Binding Proteins
/
Apoptosis
/
K562 Cells
/
Cell Proliferation
/
Metabolism
Limits:
Humans
Language:
Chinese
Journal:
Journal of Experimental Hematology
Year:
2019
Type:
Article
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