Author/Authors :
Ahn، نويسنده , , Quein and Jeong، نويسنده , , Soo-Jin and Lee، نويسنده , , Hyo-Jung and Kwon، نويسنده , , Hee-Young and Han، نويسنده , , Ihn and Kim، نويسنده , , Hyun-Seok and Lee، نويسنده , , Hyo-Jeong and Lee، نويسنده , , Eun-Ok and Ahn، نويسنده , , Kwang Seok and Jung، نويسنده , , Min-Hyung and Zhu، نويسنده , , Shudong and Chen، نويسنده , , Chang-Yan and Kim، نويسنده , , Sung-Hoon، نويسنده ,
Abstract :
We demonstrate that decursin induces apoptosis via regulation of cyclooxygenase-2 (COX-2) and survivin in leukemic KBM-5 cells. By activating an apoptotic machinery, decursin is cytotoxic to KBM-5 cells. In this apoptotic process, decursin can activate caspase family members and triggers PARP cleavage. At the same time, the expression of COX-2 and survivin in the cells is downregulated. Furthermore, decursin is in synergy with COX-2 inhibitor, celecoxib or NS398 for the induction of apoptosis. Overall, these results suggest that decursin, via inhibiting COX-2 and survivin, sensitizes human leukemia cells to apoptosis and is a potential chemotherapeutic agent to treat this disease.
Keywords :
decursin , apoptosis , COX-2 , KBM-5 , Survivin
