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目的探讨RbAp46基因对白血病细胞的作用机制。方法利用脂质体将全长RbAp46基因的cDNA片段及空载体PCB6+转入K562细胞株,分别进行生长曲线、软琼脂集落培养及细胞周期的检测,比较两者的差异。结果与空载体K562/PCB6+细胞比较,过度表达RbAp46基因的单克隆细胞株生长减慢,生长第4天,两者细胞数分别为(9.00±0.84)×105和(11.96±0.99)×105;集落减少[K562/RbAp46 vs K562/PCB6+为(131.67±15.57)vs(250.33±26.31),P<0.01];细胞周期改变主要表现为S期细胞减少[(48.88±4.35)vs(62.78±4.78),P<0.01)],G0/G1期细胞增多[(29.10±4.14)vs(22.40±2.43),P<0.05)]。结论作为抑癌基因,RbAp46通过抑制DNA合成而抑制K562细胞株的增殖。
Objective To investigate the mechanism of RbAp46 on leukemia cells. Methods The cDNA fragment of full length RbAp46 gene and empty vector PCB6 + were transfected into K562 cell line by liposome. The growth curves, soft agar colonies and cell cycle were detected respectively, and their differences were compared. Results Compared with the empty vector K562 / PCB6 + cells, the monoclonal cell lines overexpressing the RbAp46 gene were slowed down. On day 4, the numbers of the two cell lines were (9.00 ± 0.84) × 105 and (11.96 ± 0.99) × 105, respectively. (48.88 ± 4.35) vs (62.78 ± 4.78), respectively (P <0.01). The changes of cell cycle in K562 / RbAp46 vs K562 / PCB6 + were (131.67 ± 15.57) vs (250.33 ± 26.31) , P <0.01)]. The number of cells in G0 / G1 phase increased ([(29.10 ± 4.14) vs (22.40 ± 2.43, P <0.05)]. Conclusion As a tumor suppressor gene, RbAp46 inhibits the proliferation of K562 cell line by inhibiting DNA synthesis.