Effects of DLL4 gene on YY1 and c-Myc protein expression and cell proliferation in leukemia cell line K562.
- Author:
Li-Fang SHI
1
;
Hong-Bing RUI
Author Information
1. Department of Hematology and Rhematology, Fujian Medical University First Hospital, Fujian Province, China.
- Publication Type:Journal Article
- MeSH:
Cell Cycle;
Cell Proliferation;
Humans;
Intercellular Signaling Peptides and Proteins;
genetics;
K562 Cells;
Proto-Oncogene Proteins c-myc;
metabolism;
Transfection;
YY1 Transcription Factor;
metabolism
- From:
Journal of Experimental Hematology
2011;19(6):1399-1403
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to explore the effects of Notch ligand DLL4 on the protein expression of the transcription factor YY1 and proto-oncogene c-Myc, as well as K562 cell proliferation. The experiment was divided into 3 groups: normal control, negative control (pBudCE4.1-transfected) and experimental (pBudCE4.1-DLL4-transfected) groups. At 48 hours after transfection, the expression level of DLL4, YY1 and c-Myc proteins in K562 cells of each group were detected by Western blot and indirect immunocytochemical method; the CCK-8 method was used to detect proliferation of K562 cells; at 48 hours after transfection, cell cycle distribution and apoptosis of K562 cells were detected by flow cytometry. The results showed that the protein expression of DLL4, YY1 and c-Myc in K562 cells of every group were found. The protein expression levels of DLL4, YY1 and c-Myc in the experimental group cells were significantly higher than that in control groups (p < 0.05). The cell number in G(0)/G(1) phase increased in the experimental group and was higher than that in the control groups (p < 0.001), and the number of apoptotic cells were also increased (p < 0.001). It is concluded that DLL4 gene was successfully transfected into K562 cells, which increased the protein expression levels of transcription factor YY1 and proto-oncogene c-Myc, leading to the cell proliferation slower in experiment group, inducing the cell cycle arrested in G(0)/G(1) phase and increasing apoptosis.
