Abstract: To explore the synergistic mechanisms of proteasome inhibitor on TRAILinduced apoptosis in malignant lymphoma cells and to offer new ideas for clinical treatment of drug- resistant tumors. Methods: The apoptosis index, Caspase- 3 activity and Bax protein level were detected in malignant lymphoma CRL cells using flow cytometry, Western blot and fluorometry. The CRL cells were treated with PS - 341, with or without TRAIL. Results: The CRL cells were resistant to the TRAIL- induced apoptosis and the apoptosis rate of TRAIL- treated cells at 24h was only 21.3% of the level found in untreated CRL cells. Bax protein was degraded during the PS- 341 treatment and the Bax expression level at 6h was 5/9 of the level found in untreated cells. The apoptosis index increased significantly when the working concentration reached 10nmol/L PS- 341. At that concentration, the apoptosis index at 24h was 50.4%, and the expression of Bax protein was 1.2 times the level found in untreated cells. The Caspase - 3 enzyme activity was increased to 122.56 ±1.434μmol/L·h - 1·mg- 1 protein. Conclusions: Reasonable use of the proteasome inhibitor PS- 341 can effectively inhibit the degradation of the apoptotic protein Bax and reverse TRAIL resistance of malignant lymphoma cells, thus supplying a theoretical base for reasonable administration.