Hepatitis C virus and alcohol: Same mitotic targets but different signaling pathways

摘要: Background & Aims Chromosomal aberrations are frequently observed in hepatitis C virus (HCV)- and alcohol-related hepatocellular carcinomas (HCCs). The mechanisms by which chromosomal occur during hepatocarcinogenesis still unknown. However, these considered to be the result of deregulation some mitotic proteins, including alteration Cyclin B1 Aurora kinase A expression, phosphorylation gamma-tubulin. Our study aims at investigating changes expression above mentioned proteins related intracellular pathways, vitro vivo models both HCV- alcohol- dependent HCCs. Methods In this study, molecular defects involved machinery were analyzed human hepatoma cells, expressing HCV treated or not with ethanol, liver tissues from control subjects ( n =10) patients Results Expression B1, A, tyrosine-phosphorylated gamma-tubulin was reproducing infection ethanol treatment HCC cells. Interestingly, alcohol increased B, also suggest that requires PKR (RNA-activated protein kinase), as well JNK (c-Jun N-terminal kinase) p38MAPK (p38 mitogen-activated proteins; while, bypasses all pathways. Conclusions results support idea may promote oncogenesis acting through same but via different signaling