Abstract
It has been reported that microRNAs (miRs) have key roles in tumorigenesis via inhibition of their target genes. Dysregulation of miR‑27b has been detected in numerous types of human cancer, including hepatocellular carcinoma (HCC); however, the detailed role of miR‑27b in HCC has yet to be elucidated. Reverse transcription‑quantitative polymerase chain reaction and western blotting were performed to examine the mRNA and protein expression levels. Transwell assay and wound healing assay were used to determine cell invasion and migration. Luciferase reporter assay was to confirm the targeting relationship. The present study demonstrated that the expression levels of miR‑27b were significantly increased in HCC cell lines, as compared with in normal human liver cells. In addition, miR‑27b was frequently upregulated in HCC tissues, as compared with in normal adjacent tissues; the expression levels of miR‑27b were increased in 77.1% (27/35) of the HCC tissue samples. Furthermore, elevated miR‑27b expression levels were significantly correlated with tumor differentiation, Tumor Node Metastasis stage and vascular invasion (P<0.05). Knockdown of miR‑27b expression inhibited HCC cell migration and invasion. Furthermore, Sprouty 2 (Spry2) was identified as a novel target of miR‑27b in HCC HepG2 cells, and the protein expression levels of Spry2 were negatively regulated by miR‑27b in HepG2 cells. Overexpression of Spry2 suppressed HCC cell migration and invasion, whereas downregulation of Spry2 reversed the suppressive effects of miR‑27b inhibition on HCC cell migration and invasion. The results of the present study suggested that miR‑27b may promote the migration and invasion of HCC cells, at least partially by suppressing Spry2 expression. Therefore, the miR‑27b/Spry2 axis may be considered a potential therapeutic target for HCC.