二甲双胍抑制人肝癌细胞HepG2的实验研究(英文)

作者：Jing Liu; Haixia Li; Zhongcai Gao; Yuxia Wang; Wenqing Wei

来源：The Chinese-German Journal of Clinical Oncology, 2014, 13(08): 370-374.

• metformin(MET)
• human hepatocellular carcinoma cell line HepG2
• apoptosis
• cyclin D1
• reactive oxygen species(ROS)

Objective: This work aimed to study the inhibitory effect and the related mechanism of metformin(MET) on the proliferation of human hepatoma HepG2 cells. Methods: Human hepatoma HepG2 cells were treated with MET(0, 2, 10, and 50 mM). The inhibitory effect of MET on the proliferation of HepG2 cells was determined by MTT method. The apoptosis of HepG2 cells was detected by flow cytometry. The expression of cyclin D1 in HepG2 cells was examined by Western blot. ROS-DHE fluorescence probe was used to stain the reactive oxygen species(ROS) generated by HepG2 cells after treatment. Results: MET could inhibit the proliferation of HepG2 cells in a dose and time dependent manner. MET promoted the apoptosis of HepG2 cells. In addition, MET suppressed the expression of cell cycle protein cyclin D1 and induced the production of ROS in HepG2 cells. Conclusion: MET can inhibit the proliferation of human hepatoma HepG2 cells and induce cell apoptosis. Meanwhile, MET has the ability to decrease the expression of cyclin D1 and induce ROS generation, which may be involved in the mechanism of inhibiting hepatoma cells proliferation.