来那度胺对肝癌SMMC-7721细胞VEGF表达的影响

Effects of lenalidomide on vascular endothelial growth factor expression in hepatocellular carcinoma SMMC-7721 cells

目的探讨来那度胺对人肝癌SMMC-7721细胞的增殖抑制作用及其对肝癌细胞血管内皮细胞生长因子(VEGF)表达的影响。方法体外培养人肝癌SMMC-7721细胞株,分别设空白对照组和不同浓度来那度胺处理组(25μmol/L、50μmol/L、100μmol/L)。应用MTS细胞实验研究各组细胞的增殖率;采用ELISA和Western blot检测各组细胞VEGF的分泌和表达。结果细胞增殖实验显示,与空白对照组相比,不同浓度来那度胺处理组(25μmol/L、50μmol/L、100μmol/L)的增殖率分别为(78.50±6.41)%、(56.00±5.70)%、(32.51±3.52)%,差异具有统计学意义(P<0.05);ELISA结果显示,空白对照组和不同浓度来那度胺处理组(25μmol/L、50μmol/L、100μmol/L)VEGF的细胞外分泌水平分别为(88.00±4.40)pg/m L、(78.60±5.15)pg/m L、(58.27±9.10)pg/m L、(41.80±10.00)pg/m L,差异具有统计学意义(P<0.05);Western blot结果显示,随着药物浓度增加,VEGF蛋白表达水平明显下调,差异具有统计学意义(P<0.05)。结论来那度胺可能通过抑制肿瘤细胞生长、下调VEGF表达抗血管生成而发挥双重抗肿瘤的作用。

Objective To investigate the inhibitory effect of lenalidomide on the proliferation of hepatocellular carcinoma SMMC-7721 cells and its effects on vascular endothelial growth factor（VEGF） expression.Methods Hepatocellular carcinoma SMMC-7721 cells were cultured in vitro and divided into blank control group and different concentrations of lenalidomide treatment group（25 μmol/L,50 μmol/L,100 μmol/L）.The cell proliferation rate was examined by MTS assay,and the VEGF secretion and expression were determined by ELISA and Western blot.Results Compared with the blank control group,the cell proliferation rate in 25 μmol/L,50 μmol/L,100 μmol/L lenalidomide treatment groups were（78.50±6.41）%,（56.00±5.70）%,（32.51±3.52）%,respectively（P〈0.05）,indicating that lenalidomide inhibited the proliferation of tumor cells.ELISA results showed that the VEGF expression in blank control group,25 μmol/L,50 μmol/L,100 μmol/L lenalidomide treatment groups were（88.00±4.40） pg/mL,（78.60±5.15） pg/mL,（58.27±9.10） pg/mL,（41.80±10.00） pg/mL,respectively（P〈0.05）.Western blot showed that protein expression of VEGF were down-regulated in SMMC-7721 cells treated by lnalidomide in a dose-dependent manner（P〈0.05）.Conclusion Lenalidomide may play its anticancer role through inhibiting the proliferation of SMMC-7721 cells in vitro and down-regulating VEGF expression for angiogenesis.