Abstract
The present study aimed to assess the effects of the flavonoid, wogonin, and its underlying mechanism on myelodysplastic syndrome (MDS) in SKM-1 cells. In the present study, wogonin inhibited the cell proliferation of SKM‑1 cells in a dose‑ and time‑dependent manner, with the concentration required to yield a half maximal inhibitory concentration (IC50) of 212.1 µmol/l at 24 h, and 43.4 µmol/l at 72 h. Furthermore, wogonin induced cell cycle arrest at the G0/G1 phase and induced the apoptosis of the SKM‑1 cells, which possibly accounted for the antiproliferative effects of wogonin. Notably, the data in the present study revealed that wogonin upregulated the expression of p21Cip1 and p27Kip1, and downregulated the expression of cyclin D1 and cyclin‑dependent kinase 4, causing a G0/G1 phase arrest, halting cell cycle progression, and inducing apoptosis in the MDS cells, which was mediated by the mitochondrial pathway through a modulation of the ratio of Bcl‑2 to Bax. Therefore, the present study suggests that wogonin may be a logical therapeutic target in the treatment of MDS.