Objective: To investigate the influence of hepatic stellate cells( HSCs) on malignant biological behavior of hepatoma cells and related mechanisms. Methods: Human hepatoma cell lines SMMC-7721 and Hep G2,and hepatic stellate cell line LX-2 were cultured separately. HSC conditioned medium( LX2-CM),MAPK specific inhibitor U0126 were used to treat hepatoma cells,separately or together. The invasion and migration abilities of hepatoma cells were detected by TranswellTMassay,and cell proliferation was analyzed by CCK-8 assay. The mRNA and protein expression levels of p-ERK1 /2,ERK1 /2,c-Myc,vimentin and E-cadherin were determined by real-time PCR and Western blot analysis,respectively. Results: LX2-CM promoted the proliferation,invasion and migration of SMMC-7721 and Hep G2 cells,and these effects were inhibited by U0126. LX2-CM up-regulated the expression levels of p-ERK1 /2,c-Myc,vimentin and down-regulated the expression level of E-cadherin. Conversely,after U0126 treatment,the expression levels of p-ERK1 /2,c-Myc and vimentin decreased significantly,while E-cadherin expression level increased. Conclusion: LX2-CM could activate c-Myc via ERK1 /2signaling pathway in hepatoma cells,and consequently promote cell proliferation,invasion and migration,and also induce epithelial-mesenchymal transition.
Objective: To investigate the influence of hepatic stellate cells( HSCs) on malignant biological behavior of hepatoma cells and related mechanisms. Methods:Humanhepatoma cell lines SMMC-7721 and Hep G2,and hepatic stellate cell line LX-2 were cultured separately. HSC conditioned medium( LX2-CM),MAPK specific inhibitor U0126 were used to treat hepatoma cells,separately or together. The invasion and migration abilities of hepatoma cells were detected by TranswellTMassay,and cell proliferation was analyzed by CCK-8 assay. The mRNA and protein expression levels of p-ERK1 /2,ERK1 /2,c-Myc,vimentin and E-cadherin were determined by real-time PCR and Western blot analysis,respectively. Results: LX2-CM promoted the proliferation,invasion and migration of SMMC-7721 and Hep G2 cells,and these effects were inhibited by U0126. LX2-CM up-regulated the expression levels of p-ERK1 /2,c-Myc,vimentin and down-regulated the expression level of E-cadherin. Conversely,after U0126 treatment,the expression levels of p-ERK1 /2,c-Myc and vimentin decreased significantly,while E-cadherin expression level increased. Conclusion: LX2-CM could activate c-Myc via ERK1 /2signaling pathway in hepatoma cells,and consequently promote cell proliferation,invasion and migration,and also induce epithelial-mesenchymal transition.