目的： 探讨microRNA-100（miR-100）对人肝癌HepG2细胞中polo样激酶1（polo-like kinase 1， Plk1 ）表达和细胞凋亡的影响。 方法： 通过oligofectamine介导，将miR-100 mimics转染入HepG2细胞中，RT-PCR和细胞免疫荧光法检测 Plk1 mRNA和蛋白的表达，并采用AnnexinⅤ-FITC试剂盒检测HepG2细胞的凋亡情况。 结果： miR-100 mimics成功转染HepG2细胞，转染效率为（88.75±2.22）%。转染48 h后，miR-100 mimics组HepG2细胞 Plk1 mRNA的表达水平明显低于阴性对照组、空白对照组和脂质体组\[（0.71±0.01） vs （0.95±0.01）、（0.92±0.02）、（0.93±0.02），均P<0.01\]；转染72 h后，miR-100 mimics组Plk1蛋白几乎不表达，同时其细胞凋亡率明显高于阴性对照、空白对照组和脂质体组\[（26.95±6.72）% vs （15.03±512）%、（6.88±371）%、（9.00±3.37）%，均P<0.05\]。 结论： miR-100能够抑制 Plk1 基因的表达，从而促进肝癌HepG2细胞的凋亡。

Objective:To explore the effects of microRNA-100（miR-100）on expression of polo-like kinase 1 (Plk1) and the apoptosis of human hepatic carcinoma HepG2 cells. Methods: HepG2 cells were transfected with miR-100 mimics by oligofectamine. RT-PCR and immunofluorescence were used to analyze Plk1 mRNA and protein expressions in HepG2 cells, respectively. Moreover, the apoptosis of HepG2 cells was detected by AnnexinⅤ-FITC kit. Results: HepG2 cells were successfully transfected by miR-100 mimics and the transfection efficiency was (88.75±2.22) %. 48 h after transfection, the expression of Plk1 mRNA decreased significantly in the miR-100 mimics transfection group compared with the negative control, blank control, and liposome groups (\[0.71±0.01\] vs \[0.95±0.01\], \[0.92±0.02\], \[0.93±002\]，P<0.01). 72 h after transfection, Plk1 protein expression was almost undetectable in HepG2 cells transfected with miR-100 mimics. Meanwhile, the cell apoptosis rate in the miR-100 mimics group was significantly increased in comparison with those in the negative control, blank control, and liposome groups (\[26.95±6.72\]% vs \[15.03±512\]%, \[6.88±3.71\]%, \[9.00±3.37\]%, P<0.05). Conclusion: miR-100 can inhibit the expression of Plk1 gene, therefore promoting the apoptosis of hepatic carcinoma HepG2 cells.

河南省杰出青年科学基金资助项目（No. 0512000800）