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.