Abstract: Objective　To investigate the effects of luteolin on proliferation and apoptosis in K562 cells and the underlying molecular mechanism. Methods　The K562 cells in logarithmic growth phase were divided into control group, 10 μmol/L luteolin group, 25 μmol/L luteolin group, 50 μmol/L luteolin group and 100 μmol/L luteolin group, respectively. The effect of luteolin on the proliferation of K562 cells was detected by CCK8 assay, and the effect of luteolin on the apoptosis of K562 cells was detected by flow cytometry. The expression levels of Bax, Bcl-2, PARP, Cleaved-PARP, Caspase3, Cleaved-Caspase3, AKT, p-AKT and BCR-ABL were detected by Western blot assay. Results　CCK-8 assay showed that the inhibition ratio of K562 cells gradually increased with the increased luteolin concentrations and intervention time (P＜0.05). Western blot assay showed that the proliferation inhibition rate of K562 cells increased with the increased luteolin concentration and time (P＜0.05). The flow cytometry results showed that the apoptosis rates of K562 cells were increased in turn after treatment with luteolin 0, 25 and 50 μmol/L (8.21%±0.55%, 23.43%±1.50%, and 40.47%±2.97%, respectively). Western blot results showed that the expression levels of Bax, Cleaved-Caspase3 and Cleaved-PARP increased with the increasing of luteolin concentration (P＜0.05). The expression levels of PARP were increased in turn in the luteolin 0 μmol/L, 10 μmol/L and 50 μmol/L groups (P＜0.05). There were no significant difference between the 50 μmol/L group and 100 μmol/L luteolin group. The protein expression levels of Caspase3 and Bcl-2 were significantly lower in 100 μmol/L group than those in other groups (P＜0.05). The expression levels of p-AKT were lower in 50 μmol/L and 100 μmol/L groups than those in 0 μmol/L and 10 μmol/L groups. And the expression level of p-AKT was lower in 100 μmol/L group than that in 50 μmol/L group. The expression level of BCR-ABL was significantly higher in 50 μmol/L group than that in 0 μmol/L group. The expression level of BCR-ABL was significantly lower in 100 μmol/L group than that in 0 μmol/L and 50 μmol/L groups (P＜0.05). Conclusion　Luteolin can inhibit the proliferation of K562 cells and induce the apoptosis of K562 cells, which may be related to the regulation of BCR-ABL protein expression and PI3K/AKT signaling pathway.

Key words: leukemia, myelogenous, chronic, BCR-ABL positive, K562 cells, luteolin, cell proliferation, apoptosis, PI3K/AKT signaling pathway