Abstract: Objective :To study the anti-tumor effect of arsenic trioxide combining with cisplatinon the human colon cancer cells line colon26, and to explore its mechanism of interaction. Methods :The M7 method was used to obtain the ICso and the inhibition rate of the drugs on colon26 cells. The cells were stained by Acridine Orange and Propidium Iodide Fluorescence to determine the morpological alteration of apoptotic cells and the apoptotic rate. The cell cycle alteration and apoptotic rate of the cells were determined by flow cytometry. The positive rates of colon26 cells with the expression of Bcl-2 or Bax protein wire examined with flow cytometry. Results :The ICSO of cisplatin was 1.23 ml,while arsenic trioxide was 2.36 1-mol/ml Che inhibition rate of AsZOs" CDP and combinatorial treatment group tended to increase. The cells apoptotic rate was 2.68.72%,22.15±53%,24.32±14% and36.69±2.26% for the control group, Asz03, CDP and combinatorial treatment group, respectively. GZ/Mcells increased obviously in Asz03 treatment group, Go/G, cells increased in CDP treatment group, whileS cells increased in combinatorial treatment group. There was no change of Bcl-2/Bax in the CDPtreatment group or control group. Compared with AsZOs treatment group, the combinatorial treatmentgroups Bcl-2/Bax had no change. Conclusions :Arsenic trioxide of low concentration combining withcisplatin of low concentration may increase the anti- osteosarcoma effect, compare to use of arsenic tri-oxide or cisplatin of high concentration respectively, either in inhibiting colon26 cells proliferation orinducing pression apoptosis. The mechanisms of interaction are mainly that arsenic trioxide may inhibit the exof Bcl-2 protein.