Lncrna Tug1 Regulates Angiogenesis Via The Mir-204-5p/Jak2/Stat3 Axis In Hepatoblastoma

Hepatoblastoma is the most common malignant hepatic tumour type with hypervascularity in early childhood. In recent decades, emerging evidence has proven that long non-coding RNAs (lncRNAs) serve an important oncogenic role in the pathogenesis of hepatoblastoma. However, the underlying mechanism of lncRNA taurine upregulated 1 (TUG1) in the angiogenesis of hepatoblastoma remains unknown. The expression patterns of TUG1 and microRNA (miR)-204-5p were detected in hepatoblastoma tissues and cell lines via reverse transcription-quantitative PCR and were analysed using a Pearson's correlation test. A tube formation assay was performed using human umbilical vein endothelial cells to assess the vasculogenic activity of treated HuH-6 cells. ELISA was used to detect the level of the secretory proangiogenic factor VEGFA in the culture media of HuH-6 cells. A dual luciferase reporter assay was performed to validate the binding relationships of TUG1/miR-204-5p and miR-204-5p/Janus kinase 2 (JAK2). Moreover, western blotting was conducted to measure the protein expression levels of VEGFA, phosphorylated (p)-JAK2, JAK2, p-STAT3 and STAT3. It was identified that TUG1 was upregulated, while miR-204-5p was downregulated in hepatoblastoma tissues and cells. TUG1 knockdown inhibited angiogenesis induced by hepatoblastoma cells. Furthermore, miR-204-5p was identified as a target of TUG1. The results demonstrated that TUG1 attenuated the inhibitory effect of miR-204-5p on the JAK2/STAT3 pathway and promoted angiogenesis in hepatoblastoma cells. In summary, TUG1 was upregulated in hepatoblastoma and suppressed miR-204-5p, thereby activating the downstream signalling pathway of JAK2/STAT3 to facilitate angiogenesis. The present findings will provide novel targets for the treatment of hepatoblastoma.