In addition, the three Anti cancer activity of Jac A Bcl xL, Bcl 2, and Mcl 1 are overexpressed in multiple cancer cells and contribute to tumour drug resistance. Since Jac A binds to Bcl xL, Bcl 2, and Mcl 1 with high affinity and inhibits their interactions with the BH3 domain of proapoptotic proteins, we elected to study the effect of Jac A on cancer cells. Using the MTT assay, we tested www.selleckchem.com/products/Cisplatin.html the cytotoxicity of Jac A against various human cancer cell lines. Remarkably, Jac A induced a dose dependent reduction in cell viability compared to positive control doxorubicin. Jac A exhibited cytotoxic potency against breast cancer cells, colon cancer cells, lung cancer cells, liver cancer cells, and leukaemia cancer cells. Jac A showed strongest activity against leukaemia cells with IC50 values from 6.

52 to 9. 92 uM. Our results demonstrate that Jac A possesses broad anti cancer effects. In the next experiment, we tried to elucidate whether the cytotoxicity caused by Jac A is from apoptosis. K562 cells were treated with different concentrations of Jac A and the cytotoxic effects were evaluated by Annexin V and PI dual staining. Annexin V/PI staining in the control group showed a large viable cell population and a small amount of early apop totic, late apoptotic, and dead cells. Jac A resulted in a shift from viable cells to early and late apoptotic cell population with little change in the dead cell population, especially at the con centration of 10 uM. As shown in Figure 3, flow cytome try analysis showed that Jac A induced K562 cell apoptosis in a dose dependent manner.

Approximately 2. 3% 0. 9%, 9. 5% 1. 2%, 14. 4% 2. 3%, and 44. 7% 3. 3% PI AV cell populations and 1. 1% 0. 7%, 10. 2% 1. 4%, 23. 5% 3. 1%, and 22. 1% 2. 3% PI AV cell populations were detected in the 0. 1, 1, 5, and 10 uM Jac A groups, respectively. While no significant apoptotic population was detected in the control group or DMSO group. There was a significance difference in the amount of apoptosis cells in the Jac A treated groups compared with the control group. At the same conditions, the positive control Gossypol showed similar activity of induction apoptosis for K562 cells. Moreover, Jac A presented similar activity of apoptosis induction for other leukemia cells HL 60, THP 1 and colon cancer cells LOVO. After treated with 10 uM of Jac A, 33. 7% 3. 1% PI AV and 29. 2% 1. 4% PI AV cell populations were detected in HL 60 cells, and 35. 1% 2. 4% PI AV and 27. 8% 2. 1% PI AV cell populations were detected in THP 1 cells. However, the activity of apoptosis Brefeldin_A induction for LOVO cells weaker than for leukaemia cells. Only 17. 2% 1. 6% PI AV and 7. 89% 2. 2% PI AV cell pop ulations were detected in LOVO cells.