目的探讨miR-133a在不同复发时间间隔复发性肝癌中的表达差异,并研究其对肝癌细胞侵袭、迁移、增殖等生物学功能的影响。方法通过miRNA芯片筛选复发性肝细胞癌病例差异表达的miRNA;将miR-133a mimic及inhibitor转染入人肝癌细胞株SMMC-7721,通过CCK8检测细胞增殖能力,Transwell实验检测细胞迁移及侵袭能力;利用生物信息学方法预测miR-133a的可能靶基因。结果芯片结果发现miR-133a在早期复发肝癌样本中表达明显升高;转染miR-133a的mimic或inhibitor入肝癌细胞SMMC-7721后,细胞增殖能力无显著差异(P〉0.05);转染mimic后,细胞的侵袭及迁移能力明显增强(P〈0.05),而转染inhibitor后,细胞的侵袭及迁移能力明显减弱(P〈0.05)。结论 miR-133a的表达在不同复发间隔的肝细胞癌组间有显著差异,在短期复发肿瘤组织内明显升高;miR-133a可以促进肿瘤细胞的侵袭和迁移,而对增殖无明显作用,提示miR-133a水平升高可能通过促进肿瘤细胞侵袭从而增加肝细胞癌肝内转移复发风险。
Objective To investigate the expression of rniR-133a in recurrent hepatocellular carcinoma and its relation to biological functions of tumor cells. Methods Differential expression of miRNA was screened in recurrent hepatocellular carcinoma by miRNA microarray . MiR-133a mimic or inhibitor was transfected into human hepatocellular carcinoma SMMC-7721 cells. Cell proliferation was detected by CCK8 assay and cell migration and invasion was examined by Transwell assay. The bioinformatics method was used to predict possible target genes of miR-133a. Results The expression of miR-133a was significantly increased in the early-recurrent HCC. There was no significant difference in cell proliferation activity between SMMC-7721 cells transfected with miR-133a mimic and those transfected with miR-133a inhibitor ( P 〉 0. 05 ) ; however, the cell invasion and migration ability significantly enhanced ( P 〈 0.05 ) in SMMC-7721 cells after transfected with mimic, and decreased significantly after trasfected with miR-133a inhibitor (P 〈 0. 05 ). Conclusion The expressions of miR-133a is increased in hepatocellular carcinoma with early recurrence; miR-133a can promote the invasion and migration of tumor cells, and has no significant effect on cell proliferation, suggesting that elevated miR-133a levels may increase the risk of intrahepatic metastasis and recurrence of hepatocellular carcinoma.