Loss of β-catenin inhibits Stat-5α phosphorylation in bcr-abl induced leukemia cells
10.3760/cma.j.issn.1009-9921.2010.10.006
- VernacularTitle:β-catenin缺失抑制bcr-abl所致白血病细胞中Stat-5α磷酸化
- Author:
Qingchang LI
;
Chengyao XIE
;
Shuli LIU
;
Changqing FANG
;
Chen ZHAO
- Publication Type:Journal Article
- Keywords:
Leukemia,myeloid,chronic;
Leukemia,lymphocytic,acute;
β-catenin;
bcr-abl;
Wnt signalling;
Stat-5α
- From:
Journal of Leukemia & Lymphoma
2010;19(10):593-595
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the influence of β-catenin gene deletion on Stat-5α phosphorylation in bcr-abl induced leukemia cells. Methods The established conditonal hematopoitic β-catenin knockout mice were used to isolate bone marrow cells. Exogenous bcr-abl fusion gene was transduced to these bone marrow cells by retroviral infection with intent to transfom them to leukemia cells.Immunofluorescence was performed to detect the phosphorylation status of Stat-5α in both β-catenin deletion cells and control cells. bcr-abl transcription and protein levels were evaluated with real-time PCR and western blotting. Results Phosphorylation of Stat-5α was reduced significantly in β-catenin deletion leukemia cells on comparison with control cells despite that total Stat-5α protein showed no obvious changes. Total tyrosine phosphorylation and bcr-abl protein expression were reduced in bcr-abl induced β-catenin deletion CML cells,on the contrary, both of the reduction were not seen in bcr-abl induced β-catenin deletion ALL cells.Conclusion Loss of β-catenin inhibits both Stat-5α phosphorylationin and bcr-abl expression in bcr-abl induced leukemia cells.