Nuclear paraspeckle assembly transcript 1 promotes the metastasis and epithelial-mesenchymal transition of hepatoblastoma cells by inhibiting miR-129-5p
机构：[1]Department of Surgery, Children's Hospital of Soochow University, Soochow University, Suzhou, Jiangsu 215003[2]Department of Neurosurgery, The Second Affiliated Hospital of Soochow University, Soochow University, Suzhou, Jiangsu 215004[3]Department of Pathology,Children's Hospital of Soochow University, Soochow University, Suzhou, Jiangsu 215003, P.R. China[4]Institute of Pediatrics, Children's Hospital of Soochow University, Soochow University, Suzhou, Jiangsu 215003, P.R. China
The abnormal expression of nuclear paraspeckle assembly transcript 1 (NEAT1) may serve critical functions for the development and progression of various types of human tumor. However, the expression and biological function of NEAT1 in hepatoblastoma (HB) and the underlying mechanisms for the function of NEAT1 in HB remain largely uncharacterized. In the present study, the results of reverse transcription-quantitative polymerase chain reaction revealed that the expression of NEAT1 was significantly elevated in HB tissues. HB tissues with metastasis also exhibited significantly increased levels of NEAT1 compared with tissues without metastasis. The biological functions of NEAT1 were then assessed using gain-/loss-of-function studies. The results of in vitro assays revealed that inhibiting NEAT1 expression reduced the migration and invasion of HepG2 cells. By contrast, the induced expression of NEAT1 exhibited the opposite effect. The present study also demonstrated that the inhibition of NEAT1 expression prevented the epithelial-mesenchymal transition of HepG2 cells, whereas forced expression of NEAT1 exhibited the opposite effect. In addition, it was confirmed that NEAT1 could modulate the expression of microRNA (miR)-129-5p in HepG2 cells, and that NEAT1 may exert its effect on the metastatic behaviors and epithelial-mesenchymal transition of HepG2 cells by inhibiting miR-129-5p. In conclusion, the present study indicated that NEAT1 expression was aberrantly increased in HB and that it may promote the metastasis of HB cells by inhibiting miR-129-5p. Targeting NEAT1 may potentially be a novel therapeutic option for treating patients with HB.
基金：
The present study was supported by the Natural Science Foundation of China (grant no. 81502496), the Science Foundation of Jiangsu Province Health Department (grant nos. Q201503 and Q201304), Planning Project of Science and Technology Development of Suzhou (grant no. SYS201763) and the Jiangsu Government Scholarship for Overseas Studies.
