Sulforaphane Induces Apoptosis of Acute Human Leukemia Cells Through Modulation of Bax, Bcl-2 and Caspase-3

Background and Objective: Sulforaphane (SFN) is a potent chemopreventive agent obtained from cruciferous vegetables. A series of trials have demonstrated that SFN can induce cell apoptosis in a variety of tumor cells. However, the actual mechanism underlying how SFN induces apoptotic effects in tumor cells remains unclear. Current study aimed to investigate the effects of SFN on growth and apoptosis of acute leukemia cells and its molecular cascades involving in preventing tumor growth. Materials and Methods: In this study, the cell counting Kit-8 assay was used to investigate the consequences of SFN treatment on proliferation of KG1a and K562 cells to determine the appropriate drug concentration. Furthermore, the apoptosis rate of KG1a and K562 cells was assessed by FACS. The expression of Bax, Bcl-2 and caspase-3 in both cells which were affected by sulforaphane was analyzed by quantitative reverse transcription-polymerase (PCR) and Western-blotting, respectively. Results: SFN could inhibit the proliferation of KG1a and K562 cells in a dose and time dependent manner. The numbers of apoptotic cells in SFN treated groups were more than those in control group. In addition, SFN could also increase protein and mRNA expressions of Bax and caspase-3 in a dose dependent manner, but decrease Bcl-2 expression as compared to control group. Conclusion: This study indicated that SFN inhibited tumor cell proliferation and promoted apoptosis in KG1a and K562 cells through modulation of Bax, Bcl-2 and caspase-3. Current work also shed light on SFN as a promising therapeutic agent for the treatment of leukemia.