In this study, we first investigated the biological function of ANCCA/PRO2000 expression in HCC, as a critical oncogenic factor.31 Next, we provided in vitro and in vivo evidence suggesting that ANCCA/PRO2000 could not only interact with E2F2 but also negatively regulate miR-520a that inhibits E2F2 to cooperatively promote cell proliferation and tumor xenograft growth of HCC. Here, ATAD2 is linked to hepatocellular carcinoma.