The influence of ,18,F-FDG on the proliferation of HepG2 liver cancer cell was investigated and related possible mechanism was elucidated in this paper. HepG2 liver cancer cells were conventionally cultured. The cells during the phase of logarithmic growth were divided into different groups of ,18,F-FDG treatment and control groups. At 6,12 and 24h after treatment of 0—92.5×10,6,Bq/mL of ,18,F-FDG, inverted microscopy, the cell apoptosis was analyzed by use of flow cytometry and reverse transcription-polymerase chain reaction to analyze meanwhile the content of reactive oxygen species (ROS) and expression of p53 gene in cells induced by ,18,F-FDG, were determined respectively. After exposure to ,18,F-FDG, the apoptotic morphological changes of HepG2 liver cancer cells were observed. It was found that inhibition rate of cell proliferation, production of ROS and apoptosis rate increased with the radioactivity concentration of ,18,F-FDG in the range of 0—92.5×10,6,Bq/mLwhile the expression of p53 gene increased gradually. The results indicate that ,18,F-FDG may inhibit the proliferation of HepG2 liver cancer cells by apoptosis and increment of inhibition rate.