LncRNA TUG1 functions as a ceRNA for miR‐1‐3p to promote cell proliferation in hepatic carcinogenesis

BACKGROUND: Hepatocellular carcinoma (HCC) is characterised by high malignancy, metastasis and recurrence, but the specific mechanism that drives these outcomes is unclear. Recent studies have shown that long noncoding RNAs (lncRNAs) can regulate the proliferation and apoptosis of hepatic cells. METHODS: We searched for lncRNAs and microRNAs (miRNAs), which can regulate IGF1 expression, through a bioinformatics website, and predicted that lncRNA taurine‐upregulated gene 1 (TUG1) would have multiple targets for miR‐1‐3p binding, meaning that lncRNA TUG1 played an adsorption role. A double luciferase assay was used to verify the targeting relationship between lncRNA TUG1 and miR‐1‐3p. Western blotting and qPCR were used to verify the targeting relationship between miR‐1‐3p and IGF1, and qPCR was used to verify the regulatory relationship between the lncRNA TUG1‐miR‐1‐3p‐IGF1 axis. CCK‐8 was used to detect the growth activity of miRNA‐transfected L‐O2 cells, and flow cytometry was used to detect cell cycle changes and apoptosis. RESULT: The proliferation cycle of L‐O2 cells transfected with miR‐1‐3p mimics was significantly slowed. Flow cytometry showed that the proliferation of L‐O2 cells was slowed, and the apoptosis rate was increased. In contrast, when L‐O2 cells were transfected with miR‐1‐3p inhibitor, the expression of IGF1 was significantly upregulated, and the cell proliferation cycle was significantly accelerated. Flow cytometry showed that the cell proliferation rate was accelerated, and the apoptosis rate was reduced. CONCLUSION: LncRNA TUG1 can adsorb miR‐1‐3p as a competitive endogenous RNA (ceRNA) to promote the expression of IGF1 and promote cell proliferation in hepatic carcinogenesis.