Fig. 7

Proposed model for synergetic induction of apoptosis in HCC by FGFR4 and EZH2 inhibitors. Treatment with FGFR4 inhibitors alone induced EZH2 accumulation by activating NF-kB2, which maintained YAP expression levels to maintain some degree of cell proliferation-, migration- and anti-apoptosis-related genes expression, resulting in antagonism to Roblitinib. Only when FGFR4 and EZH2 were simultaneously suppressed would YAP expression and its corresponding signaling decrease sharply and eventually synergistically induce substantial HCC cell apoptosis