Open AccessAflatoxin B1 Promotes Cell Growth and Invasion in Hepatocellular Carcinoma HepG2 Cells through H19 and E2F1
Author(s) -
Jun Lv,
Yanmin Yu,
Shu-Qun Li,
Liang Luo,
Qian Wang
Publication year - 2014
Publication title -
asian pacific journal of cancer prevention
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.512
H-Index - 75
eISSN - 2476-762X
pISSN - 1513-7368
DOI - 10.7314/apjcp.2014.15.6.2565
Subject(s) - hepatocellular carcinoma , cancer research , cell growth , aflatoxin , chromatin immunoprecipitation , biology , cell , liver cancer , gene expression , gene , promoter , genetics , food science
H19 is an imprinted oncofetal gene, and loss of imprinting at the H19 locus results in over-expression of H19 in cancers. Aflatoxin B1(AFB1) is regarded as one of the most dangerous carcinogens. Exposure to AFB1 would most easily increase susceptibility to diseases such as hepatocellular carcinoma(HCC) but any possible relationship between AFB1 and H19 is not clear. In present study, we found that AFB1 could up-regulate the expression of H19 and promote cell growth and invasion by hepatocellular carcinoma HepG2 cells. Knocking down H19 RNA co ld reverse the effects of AFB1 on cell growth and invasion. In addition, AFB1 induced the expression of E2F1 and its knock-down could down-regulate H19 expression and suppress cell growth and invasion in hepatocellular carcinoma HepG2 cells. Furthermore, E2F1 over-expression could up-regulate H19 expression and promote cell growth and invasion, with binding to the H19 promoter being demonstrated by chromatin immunoprecipitation assays (ChIP). In summary, our results suggested that aflatoxin B1 could promote cell growth and invasion in hepatocellular carcinoma HepG2 cells through actions on H19 and E2F1.