Microvascular invasion in hepatocellular carcinoma overexpression promotes cell proliferation and inhibits cell apoptosis of hepatocellular carcinoma via inhibiting miR-199a expression

OBJECTIVES Long non-coding RNA (lncRNA) associated with microvascular invasion in hepatocellular carcinoma (MVIH) has been recently reported to act as a predictor for the poor recurrence-free survival of hepatocellular carcinoma (HCC) after hepatectomy. However, the biological role of MVIH in the tumorigenesis of HCC is still unclear. METHODS In the study reported here, MVIH expression levels were detected by real-time polymerase chain reaction (PCR) in tumor tissue of HCC patients and in HCC cells, including SMMC7721 and HepG2 cells. Cell viability and apoptosis were determined by MTT and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) methods, respectively. The model of transplantation tumor of HepG2 cells in nude mice was used to evaluate the effects of MVIH and miR-199a on HCC in vivo. RESULTS MVIH expression was significantly increased and miR-199a expression was significantly decreased in tumor tissue and HCC cells. si-MVIH inhibited HCC cell viability and promoted cell apoptosis, but this effect was reversed by miR-199a inhibitor. Luciferase reporter assay and RNA immunoprecipitation experiment showed that miR-199a had a direct binding ability to MVIH RNA. In nude mice with transplantation, the tumor volume was reduced by si-MVIH, and miR-199a inhibitor canceled this decrease. CONCLUSION MVIH promoted cell growth and inhibited cell apoptosis of HCC via inhibiting miR-199a expression.