摘要
目的:探讨亚砷酸对人肝癌BEL7402细胞增殖及增殖细胞核抗原(PCNA),cMyc蛋白表达的影响.方法:应用四氮唑盐(MTT)比色法、细胞群体倍增时间(TD)、细胞集落形成试验观察亚砷酸对BEL7402细胞增殖的影响,免疫组织化学法观察亚砷酸对BEL7402细胞PCNA,cMyc蛋白表达的影响.结果:亚砷酸处理后BEL7402细胞生长抑制率上升(2.0,4.0,8.0μmol/L的亚砷酸作用24,48,72h后抑制率分别为27.13%,42.65%,47.74%;35.52%,53.24%,60.41%;50.61%,65.88%,70.81%;与对照组比较P<0.05),TD逐渐延长[2.0,4.0,8.0μmol/L的亚砷酸作用48h后TD分别为(24.68±3.99);(32.42±4.46);(36.95±8.91);与对照组比较P<0.05及P<0.01],集落形成率下降(0,8.0μmol/L的亚砷酸作用7d后集落形成率分别为46.00%,18.80%;P<0.05),免疫组化结果显示亚砷酸处理后的BEL7402细胞PCNA,cMyc蛋白的表达明显减弱.结论:亚砷酸能抑制BEL7402细胞增殖,其机制可能与PCNA,cMyc蛋白的表达下调有关.
AIM: To investigate the effect of arsenious acid on the proliferation as well as the PCNA, c-Myc protein expression of HCC cell line BEL-7402. METHODS: The inhibitive effect of arsenious acid on BEL-7402 was measured with MTT and TD and the colony-forming rate of BEL-7402 cells was studied by colony-forming assay. The expression of PCNA and c-Myc protein was determined by immunohistochemical analysis. RESULTS: After treatment with arsenious acid, the inhibition rate of BEL-7402 cells increased (2.0, 4.0, 8.0μmol/L arsenious acid treatment for 24, 48, 72 h; the inhibition rate was 27.13%, 42.65%, 47.74%; 35.52%, 53.24%, 60.41%;50.61%, 65.88%, 70.81% respectively; P<0.05 vs control), TD delayed gradually (2.0, 4.0, 8.0 μmol/L arsenious acid treatment for 48 h; TD was 24.68±3.99; 32.42±4.46; 36.95±8.91 respectively; P<0.05 and P<0.01 vs control) while the colony-forming rate decreased (0, 8.0 μmol/L arsenious acid treatment for 48 h; the colony-forming rate was 46.00%, 18.80% respectively; P<0.05). In arsenious acid treated BEL-7402 cells, PCNA and c-Myc expressions were significantly down-regulated at protein level. CONCLUSION: Arsenious acid can inhibit the proliferation of BEL-7402 cells, possibly by down-regulating the PCNA and c-Myc protein.
出处
《第四军医大学学报》
北大核心
2005年第14期1303-1306,共4页
Journal of the Fourth Military Medical University
关键词
亚砷酸
肝癌细胞
细胞分裂
增殖细胞核抗原
原癌基因蛋白质C-MYC
arsenious acid
hepatocarcinoma cells
cell division
proliferating cell nuclear antigen
proto-orcogene proteins c-Myc
