Objective: To investigate the expression of microRNA-942-5p (miR-942-5p) in hepatocellular carcinoma (HCC) tissue and its functions. 
Methods: The expressions of miR-942-5p in 73 specimens of HCC tissue and paired tumor-adjacent tissue stored in the specimen bank of the First Affiliated Hospital, Xian Jiaotong University were determined by real-time quantitative PCR, and the relations of miR-942-5p expression with clinicopathologic parameters of HCC patients were analyzed. Meanwhile, the relationship between miR-942-5p expression and overall survival of HCC patients was identified by analyzing TCGA database. The changes in migration and invasion abilities of HCC cells after miR-942-5p expression interference were observed by Transwell assay. The downstream target of miR-942-5p was predicted and identified by using StarBase V3.0 database and Luciferase reporter assay, and then validated by Western blot.  
Results: The miR-942-5p expression in HCC tissues was significantly higher than that in tumor-adjacent tissue (2.390 vs. 1.764, P<0.05). The expression level of miR-942-5p was significantly associated with the number of lesions, vascular invasion and tumor stage of HCC patients (all P<0.05). The overall survival rate of HCC patients with high miR-942-5p expression was significantly lower than HCC patients with low miR-942-5p expression (19.535% vs. 53.873%, P<0.05). After silencing the miR-942-5p expression, the migration and invasion abilities of liver cancer HCCLM3 and MHCC97H cells were significantly weakened (both P<0.05). The results of prediction and analysis showed that fiblulin 5 (FBLN5) was a direct downstream target of miR-942-5p (P<0.05). Knockdown of the miR-942-5p expression led to increased expression of FBLN5 in HCCLM3 and MHCC97H cells.
Conclusion: The miR-942-5p expression is aberrantly up-regulated in HCC tissue and its overexpression is closely related to the malignant clinical features and poor prognosis. The mechanism may probably be responsible for miR-942-5p inhibiting FBLN5 expression and then promoting migration and invasion of HCC cells.