Consistently, western blotting showed that the content of cleaved Caspase3, an indicator of cell apoptosis, was significantly increased by KLF8-knockout in HCC, whereas knockdown of HMGA2 or MMP7 reversed KLF8KO-mediated Caspase3 activation (LM3 + Ctrli v.s. LM3 + HMGA2i, P < 0.001; KLF8 KO-LM3 + Ctrli v.s. KLF8 KO-LM3 + HMGA2i, P = 0.037; and LM3 + Ctrli v.s. LM3 + MMP7i, P = 0.011; KLF8 KO-LM3 + Ctrli v.s. KLF8 KO-LM3 + MMP7i, P = 0.010) (Fig. 5E, F). This evidence concerns the gene KLF8 and hepatocellular carcinoma.