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目的探讨三氧化二砷(As2O3)对人肾癌细胞系786-0的增殖抑制和诱导凋亡的作用及可能机制。方法采用细胞增殖检测、形态学观察、琼脂糖凝胶电泳和肿瘤克隆形成等方法观察As2O3对786-0细胞的增殖抑制和诱导凋亡的作用,以免疫组织化学和逆转录-聚合酶链反应(RT-PCR)技术等探讨As2O3的作用机制。结果2μmol/L以上浓度As2O3可显著抑制786-0细胞的增殖、降低细胞核分裂指数并出现凋亡的形态学改变和DNA片段化,经2.0μmol/LAs2O3处理72h后,其抑制786-0细胞增殖率为69.13%(P<0.01),使其核分裂指数由6.00降低至1.80(P<0.01),肿瘤细胞克隆形成抑制率达到100.00%。As2O3使786-0细胞内bcl-2、PCNA和Ki-67基因表达降低(P<0.01),其作用随药物浓度升高和时间延长而增加。结论As2O3对786-0细胞具有显著的增殖抑制作用,并具有浓度和时间依赖性特点,可能通过下调其PCNA和Ki-67基因表达抑制增殖,抑制bcl-2基因的表达诱导细胞凋亡。
Objective To investigate the effects of arsenic trioxide (As2O3) on the proliferation and apoptosis of human renal cell carcinoma cell line 786-0 and its possible mechanism. Methods The effects of As2O3 on the proliferation and apoptosis induction of 786-0 cells were observed by cell proliferation assay, morphological observation, agarose gel electrophoresis and tumor cloning. Immunohistochemistry and reverse transcription - polymerase chain reaction (RT-PCR) technology to explore the mechanism of As2O3. Results As2O3 at a concentration of 2μmol / L could significantly inhibit the proliferation of 786-0 cells, decrease the mitotic index, and induce morphological changes of apoptosis and DNA fragmentation. After treated with 2.0μmol / L As2O3 for 72 hours, the proliferation of 786-0 cells was inhibited (69.13%, P <0.01). The mitotic index decreased from 6.00 to 1.80 (P <0.01), and the inhibition rate of tumor cell clone formation reached 100.00%. As2O3 reduced the expression of bcl-2, PCNA and Ki-67 in 786-0 cells (P <0.01), and their effects increased with the increase of concentration and time. Conclusion As2O3 can significantly inhibit the proliferation of 786-0 cells in a time-and concentration-dependent manner. It may inhibit the proliferation of 786-0 cells by down-regulating the expression of PCNA and Ki-67 gene and inhibiting the expression of bcl-2 gene.