Effect of WISp39 on proliferation, cell cycle and apoptosis of U937 cells.
- Author:
Yue-Ying LI
1
;
Li-Qiong LIU
;
Jing YANG
;
Wei LIU
;
Xiang-Jun CHEN
;
Xiao-Qing LI
;
Wen DU
;
Shi-Ang HUANG
Author Information
1. Center for Stem Cell Research and Application, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
genetics;
Cell Cycle;
Cell Proliferation;
Cyclin-Dependent Kinase Inhibitor p21;
metabolism;
Humans;
Immunophilins;
metabolism;
RNA, Messenger;
metabolism;
Sincalide;
pharmacology;
Transfection;
U937 Cells
- From:
Journal of Experimental Hematology
2007;15(4):733-737
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the effect of a novel p21-modulating protein WISp39 on proliferation, apoptosis and cell cycle of leukemia cells, the plasmid pLenti6/V5-WISp39 was constructed and transfected into the human myelocytic leukemia cell line-U937 cells. The expression of WISp39 was detected by real-time PCR at 48 hours after transfection, proliferation of U937 cells assayed by CCK-8, apoptosis and cell cycle were determined by flow cytometry. The results showed that plasmid pLenti6/V5-WISp39 could readily enhance the expression of WISp39 in U937 cells. A significant growth inhibition (37.6%) was observed in cells tranfected with pLenti6/V5-WISp39, while the control plasmid pLenti6/V5-lacZ showed little effect on U937 growth. Further analysis revealed that pLenti6/V5-WISp39 did not show obvious apoptosis induction effect, but it could really regulate U937 proliferation via cell cycle modulation. Compared with pLenti6/V5-lacZ, pLenti6/V5-WISp39 resulted in increase of cells in G(0)/G(1) phase by 10% at 48 hours after transfection. It is concluded that the WISp39 gene has no significant apoptosis induction effect on leukemic cells, but it can increase cells at G(0)/G(1) phase via effect on cell cycle, thus inhibiting the U937 proliferation. This result means WISp39 gene can act as a negative modulator on tumour cells.
