NFKB1 and hepatocellular carcinoma: Similarly, compound 2 inhibited proliferation in HepG2, HCCLM3, and Huh–7 cells in a dose- and time-dependent manner, as well as decreased p65 subunit DNA binding capacity, p65 phosphorylation, and the consequent production of NF–κB-dependent luciferase gene expression in several HCC cell lines [33].