白藜芦醇抑制H460肺癌细胞的增殖作用研究

Inhibition effect of resveratrol on proliferation of lung cancer cells H460 by up-regulating expression of miR-622

目的探讨白藜芦醇对肺癌细胞H460增殖的影响,以探索小分子核酸miR-622在白藜芦醇抗癌中的作用。方法用不同浓度的白藜芦醇处理肺癌细胞H460,利用CCK8试剂盒检测细胞增殖,以miRNA定量试剂盒检测miR-622的表达水平。利用Lipofectamine 2000将miR-622模拟物、miR-622抑制剂及其相应对照转染进入H460细胞内。结果 50μmol/L白藜芦醇处理48 h即可使H460的细胞增殖明显降低至(49.77±1.33)%,差异有统计学意义(P<0.01)。50μmol/L白藜芦醇处理48 h后,miR-622的表达增高(13.48±2.16)倍,差异有统计学意义(P<0.01)。转染miR-622模拟物可显著提高miR-622的表达,明显使H460细胞的增殖率降低至(60.27±5.93)%,P<0.01。在白藜芦醇处理组中,转染miR-622抑制剂可明显降低miR-622的表达;与miR-622抑制剂对照组(51.67%±4.22%)相比,继而使H460细胞的增殖率增高恢复至(86.67±1.11)%,差异有统计学意义(P<0.01)。结论白藜芦醇可抑制H460细胞的生长,且这种作用与miR-622的表达上调密切相关。

Subject To investigate the inhibition effect of resveratrol on proliferation of lung cancer cell H460 by upregulating the expression of miR-622. Methods H460 cells were treated with resveratrol with different concentrations. CCK-8 assay was used for checking the proliferation in the H460 cells. The miRNA taqman assay was employed to analyze the expression of miR-622. The oligos miR-622 simulant, miR-622 inhibitor and their control were transfected into in H460 cells with aid of Lipofectamine 2000. Results The proliferation rate of H460 cells 48 hours after treated with 50 μmol/L resveratrol was significantly dropped to（49.77±1.33）%（p0.01）. The miR-622 was highly expressed by（13.48±2.16） folds in cells 48 hours after treated with resveratrol（p0.01）. Expression level of miR- 622 could be significantly enhanced after transfection of miR-622 simulant and the proliferation rate of H460 cells would significantly reduced to（60.27±5.93）%（ p0.01）. Transfection of miR-622 inhibitor could reduce the expression of miR-622 and the proliferation rate of H460 cells in resveratrol treated group would increase to（86.67±1.11）%,significantly higher than the miR- 622 inhibitor control group（51.67%±4.22%）,showing significant difference（ p0.01）. Conclusion Resveratrol can inhibit the proliferation of H460lung cancer cells and the inhibition effect might be closely related to up-regulation of expression of miR-622.