Long non-coding RNA PVT I serves as a competing endogenous RNA for miR-I86-5p to promote the tumorigenesis and metastasis of hepatocellular carcinoma

Hepatocellular carcinoma is third leading cause of cancer-related death globally. Long non-coding RNA plasmacytoma variant translocation I has been reported to be dysregulated and plays a crucial role in various cancers. In this study, we investigated the interactions between plasmacytoma variant translocation I and miR-I86-5p in the progression of hepatocellular carcinoma and explored the functional significance of plasmacytoma variant translocation I. It was determined that plasmacytoma variant translocation I was significantly higher, while miR-I86-5p was statistically lower in the hepatocellular carcinoma tissues than that in the adjacent normal tissues. Using gain-of-function and loss-of-function methods, our results revealed that plasmacytoma variant translocation I affected hepatocellular carcinoma cells proliferation, invasion, and migration. It was found that there was direct interaction between miR-I86-5p and the binding site of plasmacytoma variant translocation I by performing dual-luciferase assay and RNA immunoprecipitation assay. Furthermore, it was identified that plasmacytoma variant translocation I regulated the expression of the miR-I86-5p target gene, yes-associated protein I. Taken together, plasmacytoma variant translocation I served as an endogenous sponge for miR-I86-5p to reduce its inhibiting effect on yes-associated protein I and thus promoted the tumorigenesis of hepatocellular carcinoma.