MDM2 and hepatocellular carcinoma: Deactivation of RBM38 could promote HCC tumorigenesis and progression via promoting mdm2, then consequently inhibiting p53 and finally disrupting the p53-mdm2 loop function at the posttranscriptional level despite that p53 and mdm2 transcript amounts were stable; (2) increasing RBM38 expression could inhibit mdm2 and restore wtp53 expression in liver cancer cells, as well as (3) suppress their proliferation, growth, migration, invasion, and induce their apoptosis and senescence in vitro; and (4) increasing RBM38 expression suppressed tumorigenicity in vivo.