目的：探讨miR-96在肝细胞癌（HCC）细胞中的表达及作用。方法：用qRT-PCR测定miR-96在不同HCC细胞系（HepG2、7721、huh7）及正常肝细胞系L02中的表达；将HepG2细胞分别转染miRNA随机序列（阴性对照组）、miR-96模拟物（miR-96模拟物组）和miR-96抑制物（miR-96抑制物组）后，用细胞划痕实验及Transwell细胞侵袭实验分别检测细胞迁移及侵袭能力，qRT-PCR及Western blot分别测定PTPN9 mRNA及蛋白的表达。 结果：miR-96在各肝癌细胞系中的相对表达量均明显高于其在正常肝细胞系L02的相对表达量（均P<0.01）。与阴性对照组比较，细胞划痕愈合率在miR-96模拟物组明显升高，而在miR-96抑制物组明显降低（均P<0.05）；侵袭细胞数在miR-96模拟物组明显增多，而在miR-96抑制物组明显减少（均P<0.05）；PTPN9 mRNA与蛋白相对表达量在miR-96模拟物组均明显下调，而在miR-96抑制物组均明显上调（均P<0.05）。 结论：miR-96在HCC细胞中表达升高，并可能通过下调PTPN9表达促进HCC细胞的迁移与侵袭。
Influence of miR-96 expression on migration and invasion of hepatocellular carcinoma cells
Objective: To investigate the miR-96 expression in hepatocellular carcinoma (HCC) cells and its actions. Methods: The miR-96 expressions in different HCC cell lines (HepG2, 7721 and huh7) and normal hepatic L02 cells were measured by qRT-PCR. The HepG2 cells were transfected with scrambled miRNA sequence (negative control group), miR-96 mimics (miR-96 mimics group) and miR-96 inhibitors (miR-96 inhibitors group) respectively, and then, the cell migration and invasion abilities were examined by cell wound scratch assay and Transwell assay, and the expressions of PTPN9 mRNA and protein were determined by qRT-PCR and Western blot, respectively. Results: The miR-96 expressions were significantly higher in all studied HCC cell lines than that in normal hepatic L02 cells (all P<0.01). Compared with negative control group, the wound healing rate was significantly increased in miR-96 mimics group, and was significantly decreased in miR-96 inhibitors group (both P<0.05); the number of invading cells was significantly increased in miR-96 mimic group, and was significantly decreased in miR-96 inhibitors group (both P<0.05); both PTPN9 mRNA and protein expression levels were significantly down-regulated in miR-96 mimics group, and were significantly up-regulated in miR-96 inhibitors group (all P<0.05). Conclusion: MiR-96 expression is increased in HCC cells, which may promote the migration and invasion abilities of HCC cells by down-regulating PTPN9 expression.