中文摘要：

目的研究ROR2抑制慢性髓细胞白血病细胞株K562增殖并诱导其凋亡的作用,初步探讨可能的机制。方法采用重组ROR2腺病毒（AdROR2）感染K562细胞为实验组,重组RFP腺病毒（AdRFP）感染K562细胞为对照组。采用CCK-8法检测细胞增殖,流式细胞仪检测细胞周期变化和细胞凋亡。Western blot检测实验组和对照组促凋亡基因caspase3和抗凋亡基因survivin的表达。结果与对照组比较,实验组ROR2感染K562细胞48 h后,细胞增殖明显受抑（P〈0.05）,细胞周期主要阻滞在G2/M期（P〈0.05）,细胞凋亡增多,48 h凋亡显著（P〈0.05）,同时促凋亡蛋白caspase3表达升高（P〈0.05）,抗凋亡蛋白survivin表达下降（P〈0.05）。结论过表达ROR2能够抑制K562细胞的增殖并诱导其凋亡,其机制可能与上调了促凋亡蛋白caspase3和下调了抗凋亡蛋白survivin表达有关。

英文摘要：

Objective To determine the effect and mechanism of ROR2 on inhibiting proliferation and inducing apoptosis in chronic myeloid leukemia cell line K562. Methods ROR2 recombinant adenovirus（ AdROR2） was used to infect K562 cells（ experimental cells）,and the cells infected by RFP recombinant adenovirus（ AdRFP） served as control cells. CCK-8 assay was employed to detect the cell proliferation,and flow cytometry was adopted for cell cycle and apoptosis. The expression levels of pro-apoptotic protein caspase3 and anti-apoptotic protein were detected in both groups of cells by Western blotting. Results In 48 h after the infection of ROR2 recombinant adenovirus AdROR2,the proliferation of K562 cells was significantly inhibited（ P 〈 0. 05）,cell cycle was arrested at the G2/ M phase（ P 〈 0. 05）,the amount of apoptotic cells was increased,and cell apoptosis was obviously enhanced（ P 〈 0. 05） when compared with the control cells.At the same time,the expression level of caspase 3 was increased（ P 〈 0. 05）,and that of survivin was decreased（ P 〈 0. 05）. Conclusion Over-expression of ROR2 inhibits the proliferation and induces the apoptosis of K562 cells,which may be due to its up-regulating of pro-apoptotic protein caspase 3 while downregulation of anti-apoptotic protein survivin.