TGFBR1 and hepatocellular carcinoma: Especially, when Bel-7402-EV and Bel-7402-MUC1 cells were treated with or without different doses of exogenous TGF-β1, TGF-β1 siRNAs, JNK inhibitor SP600125 or TβRI inhibitor SB431542, we found that MUC1-induced JNK activation not only enhanced the phosphorylation of Smad2C through TGF-β/TβRI but also directly enhanced the phosphorylation of Smad2L, and then both of them collaborated to upregulate the MMP-9-mediated cell migration and invasion of HCC cells, which was consistent with the observations by Matsuzaki et al. [32, 33].