Objective     To study the canonical Wnt/β-catenin signaling of activated Wnt-3a T-lineage acute lymphocytic leukemia cell line Jurkat with recombinant adenovirus vector

observe its effect on proliferation and cell cycle progression of Jurkat cells

and investigat

e its cellular mechanism underlying acute lymphocytic leukemia.     Methods    Jurkat cells

infected with recombinant adenovirus carrying the Wnt-3a gene were divided into experimental group (Jurkat/Ad5-Wnt-3a)

empty vector group (Jurkat/Ad5-GFP)

and blank control group (Jurkat). Wnt-3a mRNA expression in Jurkat cells was detected by RT-PCR. β-catenin protein level was measured by Western blotting. Proliferation of Jurkat cells was detected by MTT assay. Progression of Jurkat cell cycle was detected by flow cytometry (FCM). c-myc and cyclin D1 mRNA expression was detected by RT-PCR.     Results    Wnt-3a was effectively expressed in Jurkat cells 48 h after transfection with recombinant adenovirus vector. Western blotting showed that the β-catenin protein level was significantly higher in experimental group than in blank control group（P0.05）. MTT assay showed that the proliferation level of Jurkat cells was markedly higher in experimental group than in blank control group 48 and 72 h after transfection with Ad5-Wnt-3a（P0.05）. FCM showed that the number of Jurkat cells at G

0

/ G

1

phase was decreased and those at  S phase was increased. RT-PCR showed that c-myc and cyclin D1 mRNA expressions  were significantly higher in experimental group than in blank control group（P0.05）.     Conclusion    Recombinant adenovirus vector-mediated Wnt-3a activates the canonical Wnt/β-catenin signaling in Jurkat cells and promotes their proliferation and cell cycle progression by down-regulating the expressions of c-myc and cyclin D1.