中文摘要：

目的 探讨视网膜母细胞瘤相关蛋白46（RbAp46）基因对白血病细胞的作用机制。方法 将全长RbAp46基因的cDNA转染人白血病细胞系K562细胞及人脑膜胶质瘤细胞系SHG44细胞，建立稳定过度表达RbAp46基因的细胞株，观察细胞的生物学行为的同时，通过RT—PCR方法寻找表达差异的相关基因。结果 过度表达RbAp46基因的K562细胞及SHG44细胞生长受抑。表现在K562／RbAp46细胞与K562／CMV细胞于生长第4天分别为（90．00±8．40）×10^4和（119．58±9．87）×10^4，SHG44／RbAp46细胞与SHG44／CMV细胞于生长第5天分别为（89．13±4．88）×10^4和（149．42±10．83）×10^4。生长第7天时，K562／RbAp46细胞和K562／CMV细胞集落数分别为131．67±15．57和250．33±26．31（P〈0．01），SHG44／RbAp46细胞和SHG44／CMV细胞集落数分别为50．78±6．77和206．67±37．18（P〈0．01）。K562／RbA046细胞与K562／CMV细胞S期细胞分别占（48．88±4.35）％和（62．78±4．78）％（P〈0．01），G0／G1期细胞分别占（29．10±4．14）％和（22．40±2．43）％（P〈0．05），而SHG44／RbAp46细胞与SHG44／CMV细胞G0／G1期细胞分别占65．6％和48．8％，S期细胞分别占22．6％和38．4％。过度表达RbAp46基因的K562细胞出现胰岛素样生长因子结合蛋白相关蛋白1（IGFBP—rP1）基因的诱导性表达。结论 在K562细胞中可能存在RbAp46和IGFBP-rP1基因之间的调控通路。

英文摘要：

Objective To explore the mechanism of action of RbAp46 gene on leukemic cells. Methods K562 leukemic cells and SHG44 glioma cells were transfected with eukaryotic expression vector carrying full-length cDNA of RbAp46 driven by the cytomegalovirus promoter mediated by lipofectamin transfection reagent. Empty vector were transfected at the same time as control. G418-resistant colonies were selected after 3 weeks culturing. Series genes were amplified using RT-PCR, Growth curve and colony formation assays were performed. Results The number of K562/RbAp46 and K562/CMV cells were （90.00 ± 8.40） × 10^4 and （ 119.58 ± 9.87 ） × 10^4, respectively after 4 days growth, and SHG44/RbAp46 and SHG44/CMV cells were （89.13 ± 4.88 ） × 10^4 and （ 149.42 ± 10.83 ） × 10^4, respectively after 5 days growth. Seven-day yields of K562/RbAp46 and K562/CMV cell colonies were 131.67 ± 15.57 and 250.33 ±26.31, respectively （P 〈0.01 ）, while those of SHG44/RbAp46 and SHG44/CMV cells were 50.78 ± 6.77 and 206.67 ± 37.18, respectively （P 〈 0. 01 ）, The fraction of K562/RbAp46 and K562/CMV cells in S phase was （48.88 ±4, 35 ） % and （62.78 ± 4.78 ） % （ P 〈 0. 01 ）, and in G0/G1 phase was （ 29.10 ± 4. 14 ） % and （ 22.40 ± 2.43 ） %, respectively （ P 〈 0. 05 ）, and that of SHG44/RbAp46 and SHG44/CMV cells in G0/G1 phase was 65.6% and 48.8%, and in S phase was 22.6% and 38.4%, respectively. Insulin-like growth factor binding protein-related protein-1 （ IGFBP-rP1 ） gene was induced to express only in the RbAp46-over expressing K562 cells and was not in SHG44 cells. Conclusion A regulatory pathway between RbAp46 and IGFBP-rP1 genes might exit in K562 leukemic cells.