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Effect of LY294002 on Wnt/β-catenin Pathway in CML Blastic Cells
Liu Zhangling, Hu Jing, Huang Zhenglan, Li Hui, Li Yajuan, Feng Wenli*
Key Laboratory of Medical Diagnostics of Ministry of Education, Faculty of Laboratory Medicine, Chongqing Medical University,Chongqing 400016, China
Abstract: β-catenin plays important roles in the progression of chronic myeloid leukemia blasts， whereas the relationship between β-catenin and the key pathways activated by BCR/ABL have not yet been elucidated. To investigate the impact of PI3K-AKT pathway on Wnt/β-catenin signal pathway， PI3K-AKT inhibitor LY294002 was used in CML blastic cells K562. Cell growth was detected by MTT test. The ability of cell colony was assessed by colony-forming assay. The protein expression of pAKT (Thr308) was detected by Western blot. The mRNA and protein expressions of β-catenin and its down-stream targets c-myc and cyclinD1 were analyzed by RT-PCR and Western blot， respectively. As a result， LY294002 significantly inhibited K562 cell growth and colony-forming ability in a dose-dependent manner. Meanwhile， the protein levels of pAKT (Thr308) and β-catenin were decreased in a dose-dependent manner after LY294002 treatment for 24 h， while the mRNA of β-catenin was not affected. Compared with the control groups， the mRNA and protein levels of c-myc and cyclinD1 were also decreased obviously after PI3K inhibitor treatment. Our data indicated that blockade of PI3K-AKT signaling inhibited the proliferation of CML blastic cells and the mechanism might be related to down-regulated expression of Wnt/β-catenin pathway.
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