Guo-Li Chen, Jianhua Liu
BACKGROUNDTensin (TNS) 4, also known as C-terminal TNS-like, is a unique oncogenic member of the TNS family that lacks the N-terminal actin-binding domain and acts as a critical signal amplifier rather than a structural scaffold. AIMTo investigate the expression of TNS4 in hepatocellular carcinoma (HCC) tissues and HepG2 and PLC cells, and its role in epithelial-mesenchymal transition (EMT). METHODSHCC and paired paracancerous tissues were collected from April 2015 to October 2017.TNS4 expression was assessed via immunohistochemistry and western blotting.Its correlation with clinicopathological features was analyzed, and Kaplan-Meier survival curves were constructed.Adeno-associated virus 8 vectors carrying TNS4-or Slug-specific shRNA were generated and used to transfect HepG2 and PLC cells.Western blotting was performed to evaluate TNS4, Slug, EMT markers, and transforming growth factor-β1/Smad pathway proteins.Cell proliferation was measured by Cell counting kit-8 assay, while Transwell and wound healing assays were used to assess invasion and migration. RESULTSExpression of TNS4 in HCC tissues was significantly higher than that in adjacent tissues (P < 0.05).The tumor-free and overall survival rates of patients with high TNS4 expression were significantly lower than those of patients with low TNS4 expression (P < 0.05).Overexpression of TNS4 promoted EMT in HepG2 and PLC cells.Silencing TNS4 downregulated expression of Slug, p-smad2 and p-smad3; reversed EMT; and inhibited proliferation, invasiveness and metastasis of hepatoma cells (P < 0.05). CONCLUSION 3 / 36High expression of TNS4 is closely related to poor prognosis in patients with HCC.TNS4 may affect Slug expression and regulate EMT through the transforming growth factor-β1/Smad pathway, and promote HCC proliferation and migration.