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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。
Objective To investigate the effect of ROR2 on proliferation and apoptosis of chronic myeloid leukemia cell line K562 and to explore its possible mechanism. Methods K562 cells were infected with recombinant adenovirusROR2 (AdROR2) and K562 cells were infected with recombinant adenoviruses (AdRFP). Cell proliferation was detected by CCK-8 assay. Cell cycle and apoptosis were detected by flow cytometry. Western blot was used to detect the expression of the proapoptotic gene caspase3 and the anti-apoptotic gene survivin in the experimental group and the control group. Results Compared with the control group, the proliferation of K562 cells was significantly inhibited (P <0.05) and the cell cycle was arrested in G2 / M phase (P <0.05) (P <0.05). At the same time, the expression of proapoptotic protein caspase 3 increased (P <0.05) and the expression of survivin protein decreased (P <0.05). Conclusion Overexpression of ROR2 can inhibit the proliferation and induce the apoptosis of K562 cells. The mechanism may be related to the up-regulation of caspase3 and the down-regulation of survivin.