Polydatin-induced cell apoptosis and cell cycle arrest are potentiated by Janus kinase 2 inhibition in leukemia cells
Polydatin-induced cell apoptosis and cell cycle arrest are potentiated by Janus kinase 2 inhibition in leukemia cells
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DOI：
10.3892/mmr.2016.4909
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发表时间：
2016-04-01
影响因子：
3.4
通讯作者：
Wan, Ding-Ming
中科院分区：
文献类型：
--
作者：
Cao, Wei-Jie;Wu, Ke;Wan, Ding-Ming
Polydatin (PD), a natural precursor of resveratrol, has a variety of biological activities, including anti-tumor effects. However, the underlying molecular mechanisms of the anti-cancer activity of PD has not been fully elucidated. The present study demonstrated that PD significantly inhibited the proliferation of the MOLT-4 leukemia cell line in a dose- and time-dependent manner by using Cell Counting Kit-8 assay. PD also dose-dependently increased the apoptotic rate and caused cell cycle arrest in S phase in MOLT-4 cells, as revealed by flow cytometry. In addition, PD dose-dependently decreased the mitochondrial membrane potential and led to the generation of reactive oxygen species in MOLT-4 cells. Western blot analysis revealed that the expression of anti-apoptotic protein B-cell lymphoma 2 ( Bcl-2) was decreased, whereas that of pro-apoptotic protein Bcl-2-associated X was increased by PD. Furthermore, the expression of two cell cycle regulatory proteins, cyclin D1 and cyclin B1, was suppressed by PD. Of note, the pro-apoptotic and cell cycle-inhibitory effects of PD were potentiated by Janus kinase (JAK2) inhibition. In conclusion, the results of the present study strongly suggested that PD is a promising therapeutic compound for the treatment of leukemia, particularly in combination with JAK inhibitors.
