H19 is an imprinted oncofetal gene, and loss of imprinting at the H19 locus results in over-expression ofH19 in cancers. Aflatoxin B1(AFB1) is regarded as one of the most dangerous carcinogens. Exposure to AFB1would most easily increase susceptibility to diseases such as hepatocellular carcinoma(HCC) but any possiblerelationship between AFB1 and H19 is not clear. In present study, we found that AFB1 could up-regulate theexpression of H19 and promote cell growth and invasion by hepatocellular carcinoma HepG2 cells. Knockingdown H19 RNA co ld reverse the effects of AFB1 on cell growth and invasion. In addition, AFB1 induced theexpression of E2F1 and its knock-down could down-regulate H19 expression and suppress cell growth andinvasion in hepatocellular carcinoma HepG2 cells. Furthermore, E2F1 over-expression could up-regulate H19expression and promote cell growth and invasion, with binding to the H19 promoter being demonstrated bychromatin immunoprecipitation assays (ChIP). In summary, our results suggested that aflatoxin B1could promotecell growth and invasion in hepatocellular carcinoma HepG2 cells through actions on H19 and E2F1.