Abstract: Objective：The BCR-ABL fusion gene induced by reciprocal translocation of t (9; 22) (q 34; q11) plays an important role in the pathogenesis of chronic myeloid leukemia (CML). Using recombinant ade -noviruses carrying the N-terminal oligomerizaton domain (OD) of the BCR/ABL and chimeric ubiquitin ligase β-TrCP, this study was to investigate the effect of the targeted degradation of oncoprotein BCR-ABL by Ubiqui -tin-Proteasome System on the proliferation of leukemia cell line K562 . Methods:The recombinant adenovirus -es carrying wi ld-type β-TrCP gene (Ad5 β-TrCP-OD-HA), mutational β-TrCP gene (Ad5 △F-TrCP-OD-HA ）and green fluorescent protein gene （Ad5GFP）were amplified in 293 cells and co-infected into K562 cells respec-tively. The rates of infection were analyzed by flow cytometry (FCM). Recombinant protein and BCR-ABL ex -pression was detected by Western blot. Cell proliferation was determined by cell counting and methylcellu-cose clonal cell culture. Cell cycle was observed through FCM. Untreated K 562 cells were used as blank con -trols. Result:The leukemia K562 cel l l ines wi th exogenous recombinant β-TrCP-OD-HA and △F-TrCP-OD-HA gene were established. The infection rates in the three groups were over 66.4% and recombinant protein sus -tained to be expressed. Ad5 β-TrCP-OD-HA down-regulated the expression of BCR-ABL and inhibi ted proliferation of K562 cells. FCM showed that the percentage of cells at S phase was decreased to 10.88%±2.42%, while that of cells at G0/G1 was increased to 85.6%±5.61%, with a significant difference (P<0.05). No changes were found in the cell cycle in groups of Ad 5 △F-TrCP-OD-HA and Ad5GFP.Conclusion:There is sustained ex-pression of recombinant β-TrCP-OD-HA protein in K562 cells infected by recombinant adenovirus. β-TrCP-OD-HA could inhibi t the prol i feration and clonogenici ty of K562 cells through targeted degradation of oncoprotein BCR-ABL and arresting the progression of cell cycle