BACKGROUND/AIMS: In recent years, a traditional Chinese medicine named Huang Qi Huai (HQH) has been frequently used in China for solid tumor therapy. However, the role of HQH on leukemia cells and its underlying mechanisms have not been elucidated. In this study, we investigated the effect of HQH on the proliferation and apoptosis of acute lymphoblastic leukemia (ALL) cell lines. METHODS: Sup-B15 and Nalm-6 cells were treated with gradient doses of HQH for 24, 48 or 72 h. Cell viability was measured using a CCK8 assay and cell cycle distribution and apoptosis levels were analyzed using flow cytometry. Western blotting was used to assess the levels of proteins associated with the apoptotic pathway. RESULTS: The results revealed that cell survival decreased significantly with increasing concentrations of HQH. HQH induced G2 cell-cycle arrest and cell apoptosis in a dose-dependent manner. HQH inhibited phosphorylated-Akt, phosphorylated- FoxO1 and Bcl2 expression and upregulated Bim, cleaved-caspase-3 and Bax expression in a dose-dependent manner, which suggests that HQH induces the apoptosis of ALL cells via the Akt/FoxO1 pathway. CONCLUSION: HQH is a potential complementary agent for the treatment of acute lymphoblastic leukemia.
BACKGROUND/AIMS: In recent years, a traditional Chinese medicine named Huang Qi Huai (HQH) has been frequently used in China for solid tumor therapy. However, the role of HQH on leukemia cells and its underlying mechanisms have not been elucidated. In this study, we investigated the effect of HQH on the proliferation and apoptosis of acute lymphoblastic leukemia (ALL) cell lines. METHODS: Sup-B15 and Nalm-6 cells were treated with gradient doses of HQH for 24, 48 or 72 h. Cell viability was measured using a CCK8 assay and cell cycle distribution and apoptosis levels were analyzed using flow cytometry. Western blotting was used to assess the levels of proteins associated with the apoptotic pathway. RESULTS: The results revealed that cell survival decreased significantly with increasing concentrations of HQH. HQH induced G2 cell-cycle arrest and cell apoptosis in a dose-dependent manner. HQH inhibited phosphorylated-Akt, phosphorylated- FoxO1 and Bcl2 expression and upregulated Bim, cleaved-caspase-3 and Bax expression in a dose-dependent manner, which suggests that HQH induces the apoptosis of ALL cells via the Akt/FoxO1 pathway. CONCLUSION: HQH is a potential complementary agent for the treatment of acute lymphoblastic leukemia.