Related Experiment Video
Updated: Jan 1, 2026

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
[Effect of CPEB4 on Proliferation and Apoptosis of Chronic Myeloid Leukemia Cells]
Xin-Yu Xu1, Li-Na Zhang1, Hui-Wen Wu1
1Technology Center, Fenyang College, Shanxi Medical University, Fenyang 032200, Shanxi Province, China.
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.
More Related Videos
Related Concept Videos
Abnormal Proliferation
Differentiation of Common Myeloid Progenitor Cells
Cell Specific Gene Expression
Inhibition of Cdk Activity

