Fig. 1

Activated HSCs or HSC-CM promoted the proliferation, migration, invasion, colony formation, and decreased the apoptosis of heat-exposed residual HCC cells. a When heat-treated residual HCC cells (Huh7, MHCC97H, Hep3B and HepG2) were co-cultured with activated HSCs LX2, proliferation was significantly higher than the cells cultured alone, as analyzed by WST-1 assay. b, c Proliferation of heat-treated residual HCC cells cultured in HSC-CM from LX2 cells was significantly higher than the cells cultured with control medium, as indicated by the WST-1 assay, BrdU-ELISA and growth curves. d PCNA and cyclinD1 mRNA expression of heat-treated residual HCC cells cultured in HSC-CM from LX2 cells were significantly higher than the cells cultured with control medium, as measured by qRT-PCR. e PCNA protein expression was analyzed by western blot. f Heat-treated residual HCC cells displayed distinct spindle-like appearance when cultured with HSC-CM from LX2 cells. g HSC-CM from LX2 cells promoted the in vitro migration and invasion of heat-treated residual HCC cells. The number of migrated and invaded cells was counted. h Colony formation of heat-treated residual HCC cells cultured in HSC-CM from LX2 cells was increased. i Apoptosis of heat-treated residual HCC cells in the presence of HSC-CM from LX2 cells was reduced than the cell cultured with control medium, as analyzed by Annexin V/PI staining. j–l The levels of Snail mRNA expression, and Snail, Vimentin, E-cadherin, and N-cadherin protein expression in heat-treated residual HCC cells cultured with HSC-CM from LX2 cells or pHSC cells compared with control medium were analyzed by qRT-PCR and western blot. pHSC primary hepatic stellate cells. **P < 0.01; *P < 0.05