Activated HSCs secrete a broad range of extracellular proteins including HGF, and aberrant HGF/cMET signaling has a critical role in bidirectional cross talk between HSCs and CACs, which promotes invasion, migration and angiogenesis in HCC.39, 40 An inverse relation in cMET and miR-199a-3p has been reported in HCC recently.28 In our study, HGF was identified as a potent target of miR-199a-3p and co-culturing of HCC cells with premiR-199a-3p-transfected HSCs dramatically attenuated migration and invasion of HCC cells through matrigel by abrogating the cross talk between HSCs and CACs. This evidence concerns the gene HGF and hepatocellular carcinoma.