摘要
目的 :观察三氧化二砷 (Arsenictrioxide ,As2 O3 )对人肾癌细胞系RCC WCS细胞生长的抑制作用 ,并初步探讨其作用机制。方法 :采用MTT法检测As2 O3 对肾癌细胞生长的抑制作用 ,用流式细胞仪检测细胞周期分布和细胞凋亡 ,用RT PCR法检测c myc和bc1 2mRNA表达的变化。结果 :As2 O3 以浓度依赖方式抑制RCC WCS细胞的体外生长 ,在浓度为 0 5、1 0、2 0和 4 0 μmol/L作用 96h时 ,As2 O3 对RCC WCS细胞的抑制率分别为 2 7 6 0 %、30 0 9%、4 1 0 3%和 5 0 77% ;与未经As2 O3 处理的RCC WCS细胞相比 ,均有显著性差异 (P <0 0 1)。As2 O3 作用后的RCC WCS细胞 ,G2 /M期细胞从 7 3%上升到 16 6 % ,同时出现 13 7%的凋亡峰。As2 O3 可以诱导c mycmRNA表达水平的下降 ,但bc1 2的表达无明显变化。结论 :As2 O3 在相当于临床应用的浓度可抑制RCC WCS细胞生长 ,使细胞阻滞在G2 /M期 ,并诱导细胞凋亡。这种抑制作用机制之一可能是诱导c myc基因表达水平的下降。
Objective:To study the effects of Arsenic trioxide (As 2O 3) on the renal cell carcinoma RCC-WCS cell line in vitro and its possible mechanism.Methods:MTT assay was used to determine the anti-proliferative effects of As 2O 3 on RCC-WCS cells. Flow cytometry was performed to evaluate the influences of As 2O 3 on cell cycle and cell apoptosis. RT-PCR was conducted to detect mRNA expression of c-myc and bc1-2.Results:As 2O 3 inhibited the growth of RCC-WCS cells in vitro in a concentration-dependent manner.Treated with As 2O 3 for 96h at the concentrations of 0.5, 1.0, 2.0 and 4.0 μmol/L, the inhibition rates of As 2O 3 on RCC-WCS cells were 27.60%, 30.90%, 41.03% and 50.77%, respectively. Compared with untreated RCC-WCS, there were significant differences at the each concentration (P<0.01). After treatment with As 2O 3,the percent of G 2/M phase of RCC-WCS cells enhanced 16.6% from 7.3%, and the percent of apoptosis was 13.7%. Treatment with As 2O 3 decreased the mRNA level of c-myc, but didnt effect the mRNA level of bc1-2 in the RCC-WCS cells.Conclusion:As 2O 3 at about the therapeutic concentrations may inhibite the growth in vitro, induce the G 2/M phase arrest and apoptosis of RCC-WCS cells. One of its possible mechanisms may be down-regulation of the expression c-myc.
出处
《临床肿瘤学杂志》
CAS
2004年第3期232-234,共3页
Chinese Clinical Oncology