Effect on the liver cancer cell invasion ability by studying the associations between autophagy and TRAP1 expression

Liver cancer is one of the leading causes of cancer associated mortality, particularly in eastern Asia. Autophagy serves an important role in carcinogenesis. Previous studies have reported that TRAP1 is a novel and efficient therapeutic target in various tumors. However, the associations between autophagy and TRAP1 is not clear. In the present study, autophagy activity and TRAP1 expression were examined in 4 different liver cancer cell lines (HepG2, Hep3B2.1-7, Sk-hep1 and HepG2.2.15) with or without rapamycin induction. The cell autophagy level was validated by monodansylcadaverine fluorescent staining, and the expression levels of Beclin1 and light chain (LC)-3-II/LC3-I. The mRNA and protein expression levels of tumor necrosis factor receptor-associated protein-1 (TRAP-1), Beclin1 and LC3-II/LC3-I were measured by reverse transcription-quantitative polymerase chain reaction, Protein Simple Western and western blot analysis. HepG2 cells, with medium invasive ability, exerted the highest basal level of autophagy and TRAP1 expression. In addition, hepatitis B (HBV) infection in HepG2 cells inhibited autophagy activity and TRAP1 expression. Rapamycin treatment also significantly enhanced autophagy in the 4 liver cancer cell lines and increased TRAP1 expression in HepG2, Hep3B2.1-7 and Sk-hep1 cells. Thus, the cell invasive ability, HBV infection and autophagy induction had different effects on TRAP1 expression, and TRAP1 may be associated with autophagy in liver cancer.